The Psychological Treatment of Depression

The psychological treatment of depression Over the past decade, Cognitive Behaviour Therapy (CBT) has become establish...

Author: J. Mar Williams

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The psychological treatment of depression

Over the past decade, Cognitive Behaviour Therapy (CBT) has become established as an effective treatment for clinical depression. Research studies throughout the world have found that CBT is as effective as the best antidepressant drugs in the short term, and that it has longer-lasting effects than medication. The Psychological Treatment of Depression describes the wide range of cognitive behavioural techniques in great detail, enabling therapists to put them to practical use. The author draws together assessment and treatment techniques of proven efficacy, describing them in usable detail, and setting them in the context of current psychological theories of depression. Some of these techniques are suitable for out-patient or primary care work, others for in-patients who may have been severely depressed for a long time. Some techniques lend themselves to long-term strategies, others to brief therapy interventions. In all cases, the techniques are explored in sufficient detail that practitioners new to CBT can feel confident about using them and that those already using them can update their skills. The final chapters discuss recent advances in research on vulnerability to depression and recent theories about what processes underlie successful therapy. Basic and clear, with explicit case studies, sample dialogues, checklists, and other helpful aids, the book is a splendid working manual, a field guide for all mental health practitioners in any discipline who want to apply or incorporate the successful methods of CBT into their work with depressed patients.


A guide to the theory and practice of cognitive behaviour therapy Second edition

J.Mark G.Williams

First published by Croom Helm in 1984 This second edition first published in 1992 by Routledge 11 New Fetter Lane, London EC4P 4EE Simultaneously published in the USA and Canada by Routledge, Chapman and Hall, Inc. 29 West 35th Street, New York, NY 10001 Routledge is an imprint of the Taylor & Francis Group This edition published in the Taylor & Francis e-Library, 2003. © 1984, 1992 J.Mark G.Williams All rights reserved. No part of this book may be reprinted or reproduced or utilised in any form or by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying and recording, or in any information storage or retrieval system, without permission in writing from the publishers. British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloguing in Publication Data A catalogue record for this book is available from the Library of Congress ISBN 0-203-41490-X Master e-book ISBN

ISBN 0-203-72314-7 (Adobe eReader Format) ISBN 0-415-06743-X (hbk) ISBN 0-415-06744-8 (pbk)

Contents

Preface to the first edition Acknowledgements for the first edition Preface to the second edition 1 Introduction

ix xi xiii 1

2 Psychological models of depression I: The behavioural background

11

3 Psychological models of depression II: The cognitive foreground

26

4 Psychological treatment of depression: Outcome studies

44

5 The assessment of depression: Some representative procedures Appendix A—Hamilton Rating Scale for Depression Appendix B—The Beck Depression Inventory Appendix C—The Cognitive Style Test Appendix D—Dysfunctional Attitude Scale Appendix E—Hopelessness Scale Appendix F—Self-Control Schedule

77 83 91 93 100 104 106

6 Treatment techniques I: Overview, basic behavioural techniques and symptom management

110

7 Treatment techniques II: Cognitive strategies

143

8 Treatment techniques III: Behavioural and cognitive therapy for chronic and unremitting depression

178

9 Training exercises

201

10 The cognitive theory of depression revisited

v

218

vi

Contents

11 Cognitive-behavioural therapy and the process of change References Name index Subject index

249 268 283 286

Tables and figures

TABLES 1.1 List of symptoms used to diagnose major depressive disorder 1.2 List of symptoms contributing to diagnosis of ‘minor depressive disorder’ 1.3 Newcastle diagnostic scale for endogenous depression 1.4 List of symptoms used by Spitzer et al. (1978) to distinguish endogenous-type depression 2.1 Summary of four behavioural formulations 3.1 Possible attributions for failing an exam 3.2 Factors in childhood history leading to depressive schemas 3.3 Schemas which occur in personality disordered patients 4.1 Treatment components in cognitive-behavioural therapies 4.2 List of variables assessed in McLean and Hakstian (1979) 4.3 Proportion of patients in remission at end of treatment 4.4 Percentage change scores on Beck Depression Inventory 4.5 Percentage of patients relapsing following initial recovery after antidepressant acute or maintenance treatment 4.6 Percentage of patients relapsing following initial recovery after acute treatment by antidepressants, cognitive therapy or the combination 6.1 Diary (to be completed each night before going to bed) 6.2 Sample list of activities for activity scheduling 6.3 Activities found by Lewinsohn to be associated with mood for 10 per cent of his sample 6.4 Activity schedule 6.5 A fear survey schedule 7.1 Thought diary 7.2 Activity and thoughts diary 7.3 List of negative thoughts for frequency ratings 8.1 Specification of problems and goals for Sarah Jane 8.2 Subcategories of verbal interactions vii

5 5 8 9 16 27 33 34 45 53 65 68 73

74 119 125 125 132 136 146 147 149 188 197

viii

Tables and figures

8.3 Reciprocal contracts negotiated by Sarah Jane and her husband Jack during marital therapy 10.1 Correlations of attributional style subscales for negative outcomes with degree of mood disturbance (MAACL) following mid-term exam results 10.2 Comparison of correlations between attributions and subsequent mood disturbances with or without exam disappointment 10.3 Beliefs that persisted after recovery from depression treated with amtriptyline

199

228

228 235

FIGURES 5.1 Possible format for daily or weekly recording of Beck Depression Inventory 92 5.2 Possible format for daily or weekly recording of Hopelessness scores 106 6.1 Diagrammatic representation of relative proportion of cognitive and behavioural techniques used as a function of stage in therapy and/or severity of depression 112

Preface to the first edition

It was not until the late 1960s and early 1970s that behavioural and cognitive approaches began to be applied in the treatment of clinical depression. Like the earlier applications of behavioural techniques for anxiety-based disorders, researchers have since used a variety of strategies to investigate efficacy and elucidate the factors affecting successful treatment outcome. Single case studies in the early writings have given way to treatment analogue studies and subsequently to larger scale outcome studies with clinical groups. There now exist several careful reviews of these studies. Although each of these points to areas in the outcome literature where there are problems in interpretation, the reviewers converge on the same conclusion: ‘Generally, behavioural and cognitive strategies can have a significant effect on depression’ (Rehm and Kornblith, 1979); ‘From these studies, there appears adequate evidence that depressives can respond to psychological intervention’ (Whitehead, 1979); ‘Several of the specific behavioural and cognitive-behavioural interventions appear to have survived initial tests of efficacy’ (Hollon, 1981). These reviewers also agree that combinations of cognitive and behavioural techniques seem to be more effective in ameliorating depression than either alone and their conclusions suggest that clinicians may be optimistic in using such techniques or combinations of techniques in their therapeutic practice; but how to proceed? The problem is that, although some techniques have rationales and procedures which have been clearly documented by their proponents (e.g. the excellent Cognitive Therapy Manual by Beck et al., 1979), this is by no means true for all the techniques which the reviewers of outcome studies cite as being effective therapeutic strategies. Some techniques which hold out clear promise as effective practices are to be found only in partial descriptions, scattered throughout the behavioural literature. When such studies are reviewed, the reviewer rarely has sufficient space to give more than one or two sentences to describe the technique under consideration. We end up knowing something of what might be most therapeutic for our clients, but little or nothing about how to go about it. It is to help fill this gap that this book has been written. ix

x

Preface to the first edition

The techniques I have chosen to describe represent a range of those currently practised by cognitive-behavioural therapists. Some are suitable for inpatient management, others more suitable for outpatient or primary care work. Some are suitable long-term strategies, others more suitable for brief therapy interventions. The therapy chapters form the central portion of the book. Their aim is to describe the techniques in sufficient detail to be useful for clinicians who want to apply such methods in their work with depressed patients, and as such, they are not written as a justification of these methods over and above alternative treatment approaches. Had space permitted it might have been possible to give details of more broad-based psychotherapeutic approaches, or of the new and challenging field of clinical ecology. (Readers interested in introductions to these fields might refer to Malan (1979) and Rippere and Adams (1982) respectively.) Unlike the arguments surrounding the growth of behaviour therapy for anxiety-based disorders, there is now a more constructive debate between proponents of different therapeutic schools. Each is more prepared to believe that patients differ in the extent to which they benefit from the techniques of the different therapeutic schools. The responsibility of practitioners of each orientation is to make plain what methods are used in their particular therapy so that individual clinicians may choose rationally which approach is appropriate for which patient. Such a description of cognitive-behavioural techniques is what is attempted as the central aspect of this book. Preceding the core therapy chapters is a chapter on assessment which gives a representative range of techniques (e.g. Beck, Hamilton) in full. The therapy chapters are followed by a section on training exercises which aims to give clinicians ideas to use in development of their own skills. The book begins and ends on a theoretical note: the first two chapters set the context for psychological approaches to depression; the last two raise some basic theoretical and research issues. I hope these more theoretical sections will be of interest to students of psychology, clinical psychology and psychiatry in their ‘abnormal psychology’ or ‘experimental psychopathology’ courses. However, the book will have fulfilled its purpose if it provides for the clinician an introduction to and encouragement to try out techniques, the utility of which can only ultimately be judged in the clinical situation itself.

Acknowledgements for the first edition

This book grew out of a series of teaching seminars and workshops I gave while at the Department of Psychiatry, University of Newcastle-upon-Tyne between 1979 and 1982. I am grateful to many people for their support, encouragement and ideas during this period, but especially to some colleagues with whom a great deal of this work was discussed: Will Barker, Anne Goodwin, Veronica Gore, Charles Lund, Angus McGregor, Ian McKeith, Jan Scott, Lindsay Shrubsole, Debbie Spaull, Stephen Tyrer and Ian Wilkinson. Since moving to Cambridge, I have been grateful for discussions with Fraser Watts, and throughout the period I have been helped by talks I have had with Chris Brewin. Secretarial assistance has been a great asset in the drafting and re-drafting of the text, and thanks are due to Sue Lowe and Gerry Mulholland in Newcastle, and to Sharon Basham in Cambridge. For permission to use their scales and questionnaires, I am grateful to Professor A.T.Beck, Professor Max Hamilton, Dr Ivy Blackburn and Ian Wilkinson. Less direct, but no less important support came at the inception of the project at work and home: at work, from Peter Britton and Donald Eccleston, colleagues whose encouragement was highly valued; at home, from my wife Phyllis, and from Robert, Jennifer, and Anne-Marie whose love and support has been a source of strength throughout. Finally, there are two people who deserve special mention; two clinical psychologists who died within a few weeks of each other at about the time this book was started; May Davidson and Roger Garside. One started me in my career as a clinical psychologist; the other was a source of valued support as a colleague when I joined the Department of Psychiatry in Newcastle. To the memory of May Davidson and Roger Garside, I should like to dedicate this book. Mark Williams

xi

Preface to the second edition

At the time of writing the first edition, cognitive behaviour therapy was still in its infancy. Over the last eight years, however, it has become established as an effective method of psychotherapy. In particular, it has led the way in promoting the use of structured psychotherapy for depressed patients as an alternative or addition to antidepressant medication. The aim of this second edition, therefore, remains that of encouraging clinicians to try cognitive and behavioural approaches with their clients. For this, therapists need not only an up-to-date review of the outcome literature, but also a clear introduction to the rationale and aim of each technique used in these studies, together with detailed description of how to proceed with each technique. The central chapters provide this information, and I have added more details on how to initiate therapy, and on how, later, to deal with underlying fears and assumptions with which patients can find great difficulty in coping. I am grateful to Arlene Weissman and to Michael Rosenbaum for permission to reproduce the Dysfunctional Attitude Scale and the Self-Control Schedule which should help assess these aspects of patients’ problems. Since the publication of the first edition, there has been extensive research on the outcome of cognitive therapy. This new edition provides an update on these developments, the most significant of which has been the finding that cognitive therapy reduces relapse. A second body of research has accumulated showing that cognitive therapy techniques, sometimes suitably modified, can be effective in helping people with chronic unremitting depression. I have included a new chapter reflecting these developments, and giving details of techniques to use in an inpatient setting. A further development has been the use of experimental cognitive psychology to help understand the process of change in psychotherapy in general, and cognitive therapy in particular. The final chapter, which is new, reviews several different attempts to understand the critical processes underlying therapeutic change, and integrates them using new findings from research on autobiographical memory and problem-solving. Finally, I have become aware that the first edition assumed a great deal of basic knowledge about the phenomenon of depression itself. The readership xiii

xiv

Preface to the second edition

of this edition turned out to be much wider than I had predicted. I greatly welcome this interest, and have written a new introductory chapter for those who may be unfamiliar with issues relating to prevalence, incidence and diagnosis of depression. Much of the new agenda for the second edition came out of workshops and training groups in Cambridge and elsewhere. I am indebted to Nacho Quemada, Gillian Rose, Simon Barnett, Peter Bentham, Keron Fletcher, Kevin Green, Paula MacKay, Steve Feast, Andy Thornton, Jane Shapleski, Katherine Foreman, Steve Jones and Ann Palmer for the helpful discussions we have shared on the practical aspects and difficulties of applying cognitive behaviour therapy. Special thanks are due to Jan Scott, Andrew MacLeod, Tracey Shea, Irene Elkin and Melanie Taylor for reading and being prepared to comment on portions of the text. Thanks, too, to Sharon Gamble for wordprocessing it all. This edition of the book was written in the last few months of my eightand-a-half years at the Medical Research Council’s Applied Psychology Unit at Cambridge. I should like to thank my colleagues there, particularly Alan Baddeley, Andrew MacLeod, John Teasdale and Fraser Watts for their support and encouragement, and for many helpful discussions on the theory and practice of cognitive approaches to emotion. It is also a fitting time to thank those who have supported me during my time in Cambridge, especially, more recently, in my role as worker-priest: Andrew McKearney, Rob and Wendy MacIntosh, Peter and Rachel Nancarrow and John and Margaret Robson. Finally, to Phyllis, my wife, and to Robert, Jennie and Annie, thanks for everything. Mark Williams Bangor 1992

Chapter 1

Introduction

A man was walking in the hills when he fell down a disused mineshaft. He fell fifteen feet, then became wedged. He dare not move lest he fall further. He cried out for help. Eventually another walker heard his cries. This walker was something of an expert at rock-climbing, pot-holing and generally getting out of fixes. Instructions were shouted down the mineshaft—where to put feet, hands and body to get into the correct position for climbing out But the man wouldn’t move. The walker muttered something about getting more help, and moved off. After some time a second walker heard the cries and came to help. This walker instantly recognized the man’s distress and confusion. He realized that the man did not have the courage to move while feeling so hopeless about his situation. So he gave him reassurance, put him at his ease, made him feel better. The man did feel better, but he was still in the mineshaft. He did not move. So the second rescuer went away to fetch more help. Eventually a third walker arrived on the scene. Like the first, he had rock-climbing experience. Like the second, he realized that the man would not make any move whilst he was so upset. Furthermore he knew two things: that the man in the mineshaft was unlikely to take the rescuer’s word for it that moving in a certain way would not make matters even worse; second, that from the top of the mineshaft it was impossible to know precisely what the man’s position was, what the risks were of moving. He would first have to ask the man to make small movements (which from experience needed to be of minimal risk) and then to ask for a report on their effects. As victim and rescuer gathered more information, the victim’s courage returned. Slowly he moved, took more risks. In time he was free. End of parable. Depression is a little like the disused mine shaft. Everyone becomes a little depressed from time to time. But sometimes, the depth of depression outweighs a person’s abilities to cope. Mood spirals downwards, the person experiences hopelessness and despair, and almost total emptiness, feels unmotivated to do many of the things they used to find enjoyable, or feels that they would rather not meet other people. It is no accident that the metaphors we used to 1

2


describe increasing severity of depression speak of ‘depth’ or ‘spiralling downwards’. Whereas anxiety ‘rises’, depression ‘deepens’. Hence the parable. The severely depressed person finds themselves trapped, in darkness, not daring to make any move for fear of making things worse, helpless about their prospect of escape. The story captures what is important about structured psychotherapies. They are not mere techniques telling a person how to get out of a bad situation, able to be taught mechanically. Neither are they merely offering a safe relationship. They aim to provide a careful combination of the two. The ‘skilled rescuer’ is the one who is able both to teach the specific things which it will be necessary for the trapped person to do in order to climb out, and to forge a relationship with the person which will give them the courage to try after so much has failed. Of course, a therapist’s personality may occasionally be sufficient so long as the person already has the necessary skills to cope with difficulty. Indeed, this may be why some placebo therapies sometimes work quite well, by encouraging those who normally use active problem-solving strategies to mobilize their skills. But for some people, dealing with their difficulties has exceeded their capacity. In this case sheer force of personality of a therapist will not be sufficient. The value of individual structured psychotherapies for depression, of which the best known are social skills training (Hersen et al., 1984; Sanchez et al., 1980), interpersonal psychotherapy (Klerman et al., 1984) and cognitive-behaviour therapy (Beck et al., 1979) is that they provide information and specific exercises for depressed patients who find they have fallen into the depths. This book describes a range of techniques. The techniques are focused around one of these psychotherapies, cognitivebehaviour therapy, but many (e.g. task assignment) are common to all structured psychotherapies. Although much of the book is concerned with ‘techniques’, the parable reminds us that these need to be embedded in a supportive relationship. Techniques are not mere mechanical devices in which certain wheels can be turned and certain responses produced. A.T.Beck and his colleagues, who have brought together many of the techniques to be described in this book under the heading of cognitive therapy, have also emphasized the qualities of empathy, warmth, genuineness and unconditional positive regard in the therapist. Appropriate and delicate use of humour, challenge, sympathy and encouragement are fundamental. Yet the research evidence suggests that the quality of the relationship is not sufficient for therapeutic progress. Studies of unstructured psychotherapy for major depression have been disappointing (see Whitehead, 1979; DeRubeis and Hollon, 1981). Furthermore if one systematically varies the subcomponents of treatment within a single session (for example, by simply exploring a negative thought, versus collaborating to challenge its validity), differences in depressed mood can be detected, despite

Introduction

3

the factor of the relationship with therapist remaining constant (Teasdale and Fennell, 1982). No book can help much in developing the personal qualities of accurate empathy into which therapists will need to embed their techniques. However, knowledge of strategies for assessing and coping with depression can help the therapist by giving him or her a clarity of perception which may better withstand the tendency to become so drawn in to the hopelessness of the patient that the therapist ends up feeling only despair and pessimism for the patient. For this reason, the techniques of assessment and of behavioural and cognitive intervention form the central aspect of this book. Exercises to use in further training, including a checklist to help evaluate one’s own developing competency as a therapist will be found in Chapter Nine. Knowledge of the techniques themselves is not sufficient. For unless a therapist has an overall framework from which the techniques are derived, they will not know in which direction to go if one approach is not proving helpful. For example, if task assignment is being used by the patient, it is important to know in what framework it is being used. Is it being used to increase the number of pleasant activities; or to increase their enjoyability (a reinforcement theory of depression); or as a homework assignment to learn social skills (a social skills framework)? Or is it being used to discover what undermining images and thoughts occur to the person when they try to engage in activities (a cognitive framework)? At different times in therapy, this same technique may serve any or all of these purposes. Without having the framework clear, the therapist is unlikely to communicate successfully to the patient what is the purpose of the assignment. Worse, the therapist will be unclear how to review the homework at the next session. If the homework has not been performed (as often happens) it makes a great difference which framework was guiding the assignment. Only on this basis can the therapist decide what the next move in therapy may be. For this reason, the next two chapters will focus on the psychological models or frameworks which underlie behavioural and cognitive approaches to depression, and the final chapters will pursue the cognitive model in greater depth. The first requirement of anyone who seeks to treat depressed patients is to know a lot about depression. It will be very important early on in therapy to allow the patient to ask questions and to be able to give answers about what depression is. I will therefore start by summarizing some of the major facts and figures about depression.

SO WHAT IS DEPRESSION? People become depressed for many reasons, for varying lengths of time to varying degrees. When depressed, different people have various ways of coping. At any one time, 4–5 per cent of a population meet the criteria

4


(detailed below) for clinical depression (Paykel, 1989). In any one year approximately one in ten of the population will have an episode of depression (Amenson and Lewinsohn, 1981). Yet most people cope without seeking treatment. Twenty-five per cent of episodes of depression last less than a month; a further 50 per cent recover in less than three months. For some, the depression may simply pass without their having to do anything. Others will have used a range of different self-help strategies (Parker and Brown, 1979; Rippere, 1977). We have already noted that 4–5 per cent of the population is depressed at any one time, but in order to give such a figure, we need to have defined clearly what we mean by ‘depressed’. The term ‘depression’ is used very often in our day-by-day conversation to describe a normal downswing of mood. Such downswings in mood may be adaptive. In rather the same way that normal anxiety and fear can warn of danger and prevent more serious harm, so depression may remind of losses and spur a person to find ways of re-engaging with activities or friends. But just as anxiety can become abnormally generalized and severe, so depression can present for the person more problems than it solves. Although the distinction is probably one of degree rather than of kind, what happens when the depression deepens is that more symptoms are ‘drawn in’. The result is clinical depression, a ‘syndrome’, that is a cluster of symptoms that tend to occur together. But these symptoms are themselves very diverse. They include emotional changes (feelings of sadness often referred to as ‘dysphoria’, the opposite of euphoria); cognitive changes (low self-esteem, guilt, rumination, memory and concentration difficulties); behavioural changes (agitation or retardation, reduced engagement in social or recreational activities) and bodily changes (sleep, eating and sexual problems, aches and pains, loss of energy). Some of these have been seen as central to a diagnosis of depression and are shown in Table 1.1. Other symptoms are excluded because, although they very commonly occur in depression, they also occur when a person has other psychological problems. For example, ‘avoidance’ occurs in phobias, and ‘ruminations’ occur in obsessions, ‘passivity’ occurs in schizophrenia and ‘irritability’ occurs in mania. Most methods of diagnosis have a number of other categories so that the many people with a wider spread of less intense (though often very persistent) symptoms may be diagnosed. Table 1.2 shows these more peripheral symptoms given by one diagnostic system. The criteria which need to be met for this mild form of depression are much more relaxed. If it were only these milder symptoms which were suffered by 5 per cent of the population at any one time, this would not be surprising. But studies of the prevalence of depression in the community have used the more stringent criteria given in Table 1.1 to assess how many people in the population are depressed. The regularity with which such studies find a figure around 4–5 per cent suggests this proportion is reliable.

Introduction Table 1.1

5

List of symptoms used to diagnose major depressive disorder (Spitzer et al., 1978)

* If one-two weeks, ‘probable’ rather than ‘definite’ diagnosis is made. ** If only four symptoms present, ‘probable’ major depressive disorder is diagnosed. Table 1.2

List of symptoms contributing to diagnosis of ‘minor depressive disorder’*

* This can be diagnosed if depression has persisted for two weeks accompanied by two or more of the symptoms listed in Tables 1.1 and 1.2 (see Spitzer et al. for details).

SEX DIFFERENCES The prevalence figures given above are not the only figures which emerge sufficiently often to be thought reliable. No less often, researchers find that the proportion of women who are depressed by these definitions exceed the

6


proportion of men (Paykel, 1989). Women are between two and three times as likely to be depressed as are men (Weissman and Klerman, 1977). The reasons for this remain uncertain. Young women with young children are particularly vulnerable and this has led some to suggest that women’s disadvantaged role with regard to opportunities for paid employment and their increased responsibility for unpaid child care is the major cause. The correlation between onset of depression, increase in life stress and the absence of social support (Brown, 1989) is wholly consistent with this conclusion. What is less clear is whether women are more vulnerable than men if they have never been depressed before. Note that studies finding sex differences are prevalence studies—that is, they are assessing the proportion of men and women who are depressed, randomly sampled from a population at a single point in time. But this does not tell us whether the depression being reported by a person is the first episode a person has ever had, or the third or the twenty-third. The excess proportion for women may arise because they are more likely to experience repeated episodes once they have been depressed, not because they were more vulnerable in the first place. There is now evidence to support this idea. Amenson and Lewinsohn (1981) carried out a longitudinal, prospective study of 1,000 people in the community. They found, as others have before and since, that the prevalence of depression was higher in women than men. But because the study was prospective, they could count what proportion of men and women became depressed for the first time during the period of the study. They found this figure (the incidence of new cases) to be 7.1 per cent for men and 6.9 per cent for women. Furthermore, they found that the episodes of depression did not last any longer in women than men, nor were women more likely to have their first episode at a younger age than men. This implies that the difference in prevalence rates arises because women who have had one episode of depression are more likely to relapse than are men who have had a similar episode. Amenson and Lewinsohn were able to confirm this. One-fifth (21.8 per cent) of women who had had a previous episode became depressed again. Although men who had been depressed before were at greater risk of future depression than those men who had never been depressed, the risk was substantially smaller than that of women. Only 12.9 per cent became depressed again. Since Amenson and Lewinsohn were careful to exclude from the analysis a large number of psychological and social factors which might have explained these sex differences, the result appears reliable. We are left with needing to explain not the increased vulnerability of women, but their increased vulnerability to repeated episodes following a first episode. We have already mentioned the stresses and potential loneliness of a child care role. This is clearly important. Another possibility is that the hormonal changes of a woman’s menstrual cycle, though not generally sufficient by themselves to bring about clinical depression, may nevertheless tend to re-activate memories and attitudes

Introduction

7

from a previous period of major depression once this has occurred for other reasons. I shall return to how such re-activation may occur in Chapter Ten, when I shall distinguish between vulnerability for a first episode, vulnerability for relapse or recurrence, and vulnerability for the episode of depression to persist.

DISTINCTIONS BETWEEN DIFFERENT SORTS OF DEPRESSION Depression is a syndrome, with clusters of symptoms which tend to occur together. In this book I shall deal only with unipolar depression—that is, with people whose depression, at times when less severe, approximates to normal mood, rather than being punctuated by periods of euphoria. In these latter cases of ‘manic depressive disorder’ or cyclothymia (the term if the mood swings are less severe), mood swings up as well as down. This is a far less common disorder, occurring in 0.5 per cent of the population. That is, about one in ten of all depressions are of this type. Although the first episode of mania can be precipitated by a life event (Ambelas, 1979) there has not yet been any systematic attempt to study the cognitive processes involved in manic depression or its implications for psychological treatment (though see Healy and Williams, 1989 for one possible account of how the biological processes underlying circadian rhythms may interact with dysfunctional attitudes and attributions to produce mania). Within the far more common unipolar depression, many attempts have been made to identify subclusters of symptoms within the syndrome. The distinction which has aroused most controversy, yet become most firmly embedded within psychiatric thinking, is that between endogenous and reactive depressions. The distinction was originally intended to capture the difference between those whose depression arose ‘from the inside’ (from biochemical disturbance in the brain) and separate them from those who were depressed in reaction to external stresses (sometimes called ‘exogenous’ to parallel the term endogenous). Yet from the earliest days of research in this area, many more differences than simply ‘presence or absence of a life event’ were taken into account when deciding whether the depression was ‘endogenous’ or ‘reactive’. One of the ways of assessing endogeneity which has lasted longest was derived from a list of symptoms and their weightings derived in a study which examined response to electro-convulsive therapy by Carney et al. (1965) (see Table 1.3). This ‘Newcastle Scale’ is still widely used in diagnosis today. But is it a reliable and valid distinction that is being made? Other statistical analyses suggest that, if there are subclassifications to be made, they are more complex than endogenous-reactive. One such analysis identified four categories: anxious depression, hostile depression, retarded depression and agitated depression (Overall and Hollister, 1966). Another

8

The psychological treatment of depression Table 1.3

Newcastle diagnostic scale for endogenous depression (Carney et al., 1965)

such analysis is that by Young et al. (1986) who also found four groups distinguished by two dichotomous features: the presence or absence of anhedonia (lack of ability to experience pleasure) and the presence or absence of ‘vegetative’ features (e.g. changes in sleep and appetite). It is certainly the case that endogenous depression is preceded by stressful life events as often as other depressions are (Paykel, 1989). Studies which appear to show that non-endogenous patients have experienced more life events have relied on self-report rather than independently checked events. Such self-reports can be unreliable (Robins et al., 1990). This has encouraged some to suggest that the term ‘endogenous’ should only be taken to describe a certain cluster of symptoms, and not be taken to refer to how the depression was caused. The result of this is that when the word endogenous is used nowadays, it most commonly refers to cases where certain features are found (see Table 1.4). Other cases are simply called ‘non-endogenous’ so as not to imply that all other cases are reactive. One might have expected that clarifying the term in this way would have helped research into the biological factors which may be causal in depression. In particular much research effort has gone into the search for biological markers (bodily signs indicating the level or integrity of a biological system). Although discussion of this research is beyond the scope of this book, progress in this area appears to have been disappointing. For example, early hopes for the Dexamethasone Suppression Test (DST) have foundered. In this test, dexamethasone is given to patients to see if the mechanism which controls natural cortisol output in the body is shut down or suppressed (as it should) by the presence of dexamethasone. Although non-suppression occurs more often in endogenous patients than in non-endogenous (showing that the hypothalamic-pituitary-adrenal system is faulty) it is not unique to endogenously depressed patients. Non-

Introduction Table 1.4

9

List of symptoms used by Spitzer et al. (1978) to distinguish endogenous-type depression

suppression has also been found in mania, in schizophrenia, in dysthymic patients and in patients with anorexia nervosa. Indeed, some have suggested that the fault in the hypothalamic pituitary system could be secondary to other factors such as weight loss (see Free and Oei, 1989 for more extended discussion of this issue). This has made a recent report conclude: ‘The initial DST status does not powerfully or consistently supplement clinical methods of diagnosis of major depression for predicting short-term responses to adequate doses of tricyclic antidepressants or ECT’ (APA Task Force on Laboratory Tests in Psychiatry, 1987:1257). But does the endogenous/non-endogenous subtype difference relate differently to psychological variables? The small number of studies which have been done give a slightly mixed picture, the evidence weighted against the distinction being important. DST non-suppressors are equivalent to DST suppressors in questionnaire measures of dysfunctional attitudes (Rush, 1983; Norman et al., 1987). In one recent study Robins et al. (1990) found that dysfunctional attitudes measured by the Dysfunctional Attitude Scale (DAS) (Weissman and Beck, 1978) was significantly lower in endogenous patients than non-endogenous (distinguished on the Research Diagnostic Criteria). However, in another recent study of our own, we found that endogeneity assessed by the Newcastle Scale did not correlate with dysfunctional attitudes (Williams et al., 1990).

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Studies of response to cognitive behavioural treatment have found a similar picture: that endogeneity does not predict response. Blackburn et al. (1981), Kovacs (1981) and Beck et al. (1985) looked to see if the presence of endogenous symptoms made patients any less likely to respond to cognitive therapy. They did not. Note, however, that these studies (as with most other outcome studies of cognitive therapy that have been done) excluded psychotically depressed patients (i.e. those who had delusions and/or hallucinations); and have used outpatients, thereby excluding the most severely depressed hospitalized patients. The definition of endogenous can be either lax or relatively restrictive (for example, both the DSM IIIR definition of major depression, melancholic subtype and the older Newcastle Scale are more restrictive than the endogenous category of Spitzer et al.’s (1978) Research Diagnostic Criteria), and no study of more severe inpatient depressives has been large enough to see if using a more restrictive definition would predict treatment response. As psychological treatments move further towards treating more severe patients, it would be well to keep an open mind on whether diagnostic distinctions will be helpful. Although subtype differences may well turn out to represent markers of severity (Kendall, 1976), it remains true that several studies have found that patients with ‘endogenous’ symptom clusters differ in several respects from patients without such symptoms. They differ in their style of rumination (Nelson and Mazure, 1985), in the content of their thoughts (Matussek and Luks, 1981), in the ease with which distraction can reduce their negative thinking and mood (Fennell et al., 1987) and the ease with which imagery techniques can help compensate for poor concentration and memory (Watts et al., 1988). Though these differences may not be reflected in overall response to psychological treatment, they may be determining which techniques within a therapy package are most helpful for different kinds of patient. Such information is evidently of value in discovering which procedures will best meet the needs of which patient. Discussion of the nature of depression has brought us full circle to treatment issues. That is not surprising. The most important aspect of any clinical syndrome (no less true of other aspects of our environment such as tables and chairs) is not so much what it is ‘in itself’—its essence—but how it responds when you do something to it. This book is not about ‘doing something to’, but it is about doing something for and with depressed people. We start, in the next two chapters, by describing the psychological frameworks that underlie the cognitive-behavioural therapy approach.

Chapter 2

Psychological models of depression I The behavioural background

In the 1960s and early 1970s, clinical psychologists concerned themselves mostly with the behavioural treatment of anxiety-based disorders: phobias, obsessions and general anxiety. Where other problems were tackled, it was because they were assumed to have an anxiety component, e.g. tics, stammering, sexual problems. Careful analysis of the situations in which the anxiety arose, followed by relaxation, desensitization, exposure, response prevention, massed practice, etc.—these were the staple diet of the behavioural practitioner. Somehow, depression was not thought the appropriate target for such interventions. Firstly, depression appeared more ‘biological’, and if so the behavioural aspects would be mere symptoms. The development of antidepressant drugs had appeared to confirm the theory that depression was the result of deficiencies in some combination of biogenic amines in the brain. Secondly, although some depression was thought ‘reactive’, where the trauma was great, the depressive response seemed understandable and not requiring any special theory. Where the trauma was little, and the depressive response apparently out of proportion, there were psychodynamic explanations available. Thirdly, the symptoms of depression are many and various. The earliest behavioural speculations about depression had spoken of depression as ‘extinction’ (behavioural repertoire being weakened due to insufficient reinforcement relative to the effort expended—the response cost). Yet such notions did not seem to do justice to the variety of symptoms in depression. Indeed, as we saw in the last chapter, a person may be diagnosed depressed on the grounds of low mood, suicidal ideas, appetite disturbance, sleep disturbance, feelings of self-reproach and concentration or memory problems, without reduced behavioural output or ‘extinction’ being a major feature. Yet it is with such behavioural formulations that this review of the background to cognitivebehaviour therapy must start. Whatever their deficiencies as complete explanations of the phenomena of depression, they were arguably the most significant development in clinical psychological theorizing since the interpretations of phobic reactions as conditioned emotional responses earlier in the century. They broke the mould of predominant explanations for 11

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depression: the biogenic amine theory on the one hand and the psychodynamic theory on the other. I shall start by reviewing some early behavioural formulations, and then trace their more recent development Finally we shall see how the theory of learned helplessness builds a bridge from behavioural towards cognitive approaches.

EARLY BEHAVIOURAL FORMULATIONS Reduced frequency of social reinforcement Early behavioural formulations of depression attributed the symptoms to ‘inadequate or insufficient reinforcement’ (Lazarus, 1968). However it was not clear whether ‘inadequate’ implied reduced frequency or quality of reinforcement. By contrast, theories which spoke of reduced frequency of social reinforcement were more specific. ‘Frequency’ is a particular concept and ‘social’ limits the otherwise wide term ‘reinforcement’. It is a theory most often associated with Lewinsohn (e.g. Lewinsohn et al., 1970). According to Lewinsohn, low rate of response contingent positive reinforcement has consequences in terms of the respondent behaviour of the individual (elicits crying, dysphoric mood, etc.) and is itself sufficient explanation for reduced behavioural output in depression. In the early stages of depressive breakdown, symptoms may be maintained by reinforcement from others (the ‘secondary gain’ phenomenon), but later on close family and friends are more likely to stop rewarding the person’s behaviour. They may try to avoid the depressed person altogether, thus further reducing frequency of rewards available in the environment. However the concepts are not so circumscribed as may be supposed. The concept which is important but missing is that of the SD, the ‘discriminative stimulus’ (Ferster, 1966). This is the stimulus in the environment which signals the availability of reinforcers in rather the same way in which a laboratory animal may learn that food will only be available when a small light is on, and then only when it presses a bar. If a person were to become less sensitive to stimuli in the environment which normally ‘announce’ the availability of rewards, then the effect on behaviour would presumably be the same as reducing frequency of actual reinforcement. These are very different models, but are almost indistinguishable solely on the basis of their behavioural effects. Furthermore, ‘reduced reinforcement’ paradigms are too narrow. A truly comprehensive theory would include a greater number of parameters of reinforcement—frequency, duration, magnitude and the amount of behaviour required to obtain the reinforcer (the response cost).

Psychological models of depression I

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Loss of reinforcible behaviour This theory is ascribed to Ferster (1966, 1973) and refers to the reduction of reinforcible behaviour in the repertoire (for any reason). Simply put, if the behaviour is not there to be rewarded, it will not be rewarded. Such reduction in behaviour characteristically follows large and/or sudden environmental changes, which change the stimulus conditions which normally control behaviour. It may also result from reinforcible behaviour being squeezed out of the repertoire by the need to escape or avoid stress, or by increase in hostility which reduces other people’s willingness to give ‘social reinforcement’. Clearly this formulation is very similar to those of ‘inadequate or insufficient reinforcement’ mentioned above. Aversive control This theory attributes reduced behavioural output to the fear that anything a person does will be punished. Although several authors have pointed out that depression may result from unusually intense and prolonged anxiety (Lazarus, 1968; Wolpe, 1972) this is different from explaining actual performance deficits in depression in terms of expectations of unpleasant consequences. This is despite the fact that (although anxiety and depression are distinguishable as clinical syndromes), anxiety is very often a component in the depressive state, especially in mild depressions. The significance of ‘punishment’ or ‘stimuli signalling punishment’ becomes more clear if Gray’s analysis of their equivalence with ‘frustrative non-reward’ and ‘stimuli signalling frustrative non-reward’ (respectively) is borne in mind (Gray, 1987, 1990). In the circumstances of bereavement, for example, the individual is besieged by stimuli which have normally signalled the presence of their loved one: ‘the alarm clock which he always turned off’, ‘the television programme she always used to watch’ and so on. Yet the person is not there when they look around—paradigmatic of ‘frustrative non-reward’. Many of the stimuli in the environment must thereby become signals for such non-reward, and reduction in behaviour ensues as certainly as if the behaviour was being systematically punished. This formulation seems inadequate to explain the generalization of behavioural deficits in depression, yet if one extends the theory to include ‘conditioned inhibition’— the reduction in behavioural output owing to the presence of stimuli signalling that no reward is available—it may yet explain a wide range of phenomena. Loss of reinforcer effectiveness According to this theory (Costello, 1972a) sufficient reinforcers may be available in the environment and the individual might still be capable of procuring them, but for some reason they have lost their potency as reinforcers. This is in contrast with those theories which would predict that only techniques

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which increase total amount of rewarding events or those which teach the necessary skills (e.g. assertion training) to procure such rewards will ultimately be effective in alleviating depression. The formulation seems particularly useful in accounting for depressions which do not seem to follow any loss event (and although many do, a substantial minority do not). It also seems to account for the finding by people who are depressed that their discomfort and dysphoria may be increased when they attempt to do things which they formerly found pleasurable—an aspect of the syndrome which has been ignored by many theorists. If individuals expect from past experience to get pleasure from an activity then they find it is not rewarding, a frustrative nonreward effect will follow, increasing discomfort accordingly. How does loss of reinforcer effectiveness come about? According to Costello, it may result from endogenous changes in the biochemical mechanisms known to underlie consummatory motivation, or it may result from the disruption of a behavioural chain by the loss of a single reinforcer in that chain. It is this latter behavioural formulation which is potentially of interest to the psychological therapist. It sounds rather as if a single loss may have general consequences by its chain disrupting effects, in rather the same way as a housebuying chain of several agreements may be upset by the disruption of one purchase in the chain. The difference here is that all the ‘contracts’ are being made within the behavioural repertoire of a single individual. Put differently, the stimuli, responses and reinforcers in a person’s behaviour are mutually interdependent (Costello, 1972b), and it may be that some people’s greater proneness to depression reflects the fact that the mutual interdependence of their behaviour is particularly strong and needs to be weakened It resembles most closely the clinical observation of an individual ‘putting all their eggs in one basket’. A patient who says ‘If I can’t have my lover back, there is nothing for me’ is defining all rewards in terms of a dependence on one particular state of affairs—a state of affairs over which they may have little control in any case. A person who has a ‘network’ of rewards which is dependent on one or two central components (be it love, job, status, children), is vulnerable to disruption in the chain and as a consequence to generalized loss of reinforcer effectiveness. Eastman gives a helpful analogy: Consider a tightly stretched net, made of some elastic filament. The knots in this net represent behaviours, stimuli and reinforcers, while the filaments between them represent the interdependencies. If a single knot is excised, a large hole appears: the net effectively collapses. This represents the disruption of the relationships between behaviours, stimuli and reinforcers that Costello calls a ‘loss of reinforcer effectiveness’. If the net is only loosely stretched in the first place and if there are inbuilt holes (some behaviours, etc. are not interrelated with others), then the removal of one knot will have only a small effect on the total. (Eastman, 1976:282)


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EVALUATION OF EARLY BEHAVIOURAL FORMULATIONS Table 2.1 shows a summary of the four behavioural formulations, set out according to the factors which render a person vulnerable to, which precipitate or which maintain the depression. What is the evidence that these models are valid? Up until the early to mid-1970s there was very little evidence. The problem was that these models were not expressed sufficiently precisely to generate testable experimental or clinical predictions. Even the more precise formulations, which generated the greatest amount of evidence, suffered from the problem of correlational evidence. Take, for example, the ‘reduced frequency of social reinforcement’ model of Lewinsohn and his co-workers in Oregon. Their theory is broadly as laid out in Table 2.1, and has vulnerability (lack of interpersonal skills), precipitating (loss event), and maintaining (inadequate or insufficient response contingent positive reinforcement) components. Many writers have pointed out the insufficiency of correlational data in establishing this model. The fact that fewer activities are associated with low mood does not imply that the behaviour changed prior to the mood. Indeed, Lewinsohn’s own practice in obtaining these correlations would easily allow the opposite to be the case. This is because, in asking subjects in his experiments to rate the number of activities which occurred on any particular day, they are always instructed in a daily frequency check to count an activity as having occurred only if it was ‘at least a little pleasant’. For example, if watching television is on a subject’s activity schedule, then if TV-watching was not experienced as enjoyable (a common occurrence) the subject does not check that particular activity on that day (Lewinsohn, 1975). Small wonder then that Lewinsohn and his colleagues obtain significant correlations between subjects’ daily ratings of frequency of activities and daily mood ratings. On a ‘good day’ (assuming affective state to be prior) a subject will enjoy more activities, so his ‘frequency’ rating will rise. It is not valid to conclude from correlations thus obtained that rate of behavioural output is prior to affective change. (Sanchez and Lewinsohn (1980) have, as I shall report later, attempted to address the issue of causal primacy between mood and assertive behaviour, but there are problems in interpreting even these data.) In the following section, I shall review research on those models which have become precise enough to gather evidence for and against them. Although each has been concerned with the central aspect of ‘adequate reinforcement’ for the maintenance of behaviour, each has focused on different aspects. Social skills theory, the most direct successor to the earlier formulations, continued to emphasize the reduced frequency of social reinforcement. The second, selfcontrol theory emphasized the depressed person’s inability to reinforce their own behaviour. The third, learned helplessness, focused not on the reduction of reinforcement, but rather on the independence between behaviour and reinforcement.

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Table 2.1 Summary of four behavioural formulations

SOCIAL SKILLS DEFICITS IN DEPRESSION Early descriptions in the literature certainly seemed to support the view that depressed people have social skills deficits. The observations of Lewinsohn and co-workers (Lewinsohn et al., 1970; Libet and Lewinsohn, 1973) seemed to indicate that depressed individuals differed from non-depressed individuals in at least five areas: the total amount of verbal behaviour; the number of times the individual initiated behaviour (i.e. not a reaction to another); the degree to which the individual distributed their behaviour equally towards a group of others; the latency to respond to behaviour of another; and the rate of positive/reinforcing behaviour. The problem with these conclusions was that they were largely derived from uncontrolled observations of depressed individuals in their homes (where the entire interpersonal structure may be biased as much by the ‘non-depressed’ family members as by the behaviour of the ‘depressed’ individual). Other data were derived from observations of groups of depressed individuals without extensive comparisons with non-depressed subjects.


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Whether one judges these initial descriptions to be right or wrong depends on how one defines social skills. Social skills have been assessed in many different ways from ‘molecular’ to ‘molar’ aspects: observer ratings of the minutiae of behaviour (e.g. eye contact, head nods, etc.); observer ratings of number of positive and negative actions and reactions; self-monitoring of such positive and negative actions/reactions; structured interviews of interpersonal adjustment; and self-ratings of difficulty with interpersonal situations. Different definitions and different methods of assessment produce different results. For example, Coyne (1976) found that depressed individuals had a marked alienating effect on people to whom they were talking in a twenty-minute telephone conversation, but apart from the length of time the depressed person spent talking about themselves, the precise measures of social behaviour (total amount of speech, number of approval responses such as ‘yeah’, ‘hm-hmm’ and ‘yes’, number of hope statements, and degree of ‘genuineness’) did not distinguish depressed from non-depressed patients or control subjects. A similar conclusion emerged from a very careful analysis of social interaction in depression by Youngren and Lewinsohn (1980). They examined the behaviour of seventy-five neurotically depressed outpatients in comparison with sixty-nine non-depressed psychiatric controls and with eighty normal controls. On five subscales of the Interpersonal Events Schedule (social activity, assertion, cognition, give positive and receive positive) the depressed patients rated themselves as less skilled than did normals and non-depressed psychiatric controls, consistent with ratings made by peers and by independent coders. However, the independent observers found no difference between depressed and non-depressed patients in the minutiae of social behaviour: activity level, initiation level, actions elicited, positive reactions elicited, negative reactions elicited, speech rate, speech volume, eye contact, smiling, facial expression and gestures (illustrators vs adaptors). Similarly, Lewinsohn and Amenson (1978) assessed a number of specific categories of overt behaviour but found that only the more global ratings tended to differentiate depressed patients, and to be associated with therapy improvement. A further study by Kornblith et al. (1983) also found that improvements in general ratings of depression over twelve weeks of self-control therapy were not paralleled by any changes in specific social behaviour. Only one study appears to have shown differences between depressed patients and non-depressed controls in social skills at the ‘molecular’ level (Bellack et al., 1983). From a careful analysis of videotaped role-plays of eight positive and eight negative scenarios, they found differences on speech duration, voice tone, gaze, posture, request/compliance content and overall assertiveness. Note however that of these, only speech duration was objectively measured, the remainder were subjective ratings on five-point bidirectional Likert-type scales. There were in fact two other measures made objectively

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(response latency and number of smiles) and neither of these differed between the depressed and non-depressed group. Added to the fact that these behaviours were assessed in role-play situations, whereas Coyne (1976), Youngren and Lewinsohn (1980) and Kornblith et al. (1983), who found no molecular differences, took observations from genuine interactions, it can at least be said that the level of specific skills elements has not so far yielded as sensitive a measure of interpersonal difficulty as do more global ratings of behaviour. But if the patients and observers agree that there is something wrong with the interpersonal behaviour of depressives, and if these errors cannot be detected at the molecular level, where do they originate? I have already referred to Coyne (1976), who studied twenty-minute telephone conversations in forty-five subject pairs. One member of each pair was an undergraduate subject, the other member of the pair (the target) was either a depressed patient (N=15) or a non-depressed patient (N=15) or a non-depressed control subject matched for age and social class with the patients (N=15). All subjects in the experiment were women. Results showed that the non-depressed subjects felt more depressed, anxious and hostile following interaction with depressed patients than after interaction with non-depressed patients or controls. They also wished to have significantly less future contact with these individuals. Furthermore, there were significant associations between mood disturbance following the conversation and extent of rejection of opportunities for further contact. It was found that the depressed subjects spent more time talking about themselves (talking freely of deaths, marital infidelities, hysterectomies, family strife and ‘a variety of other intensely personal matters’). In the absence of measurable differences in the elements of the interaction Coyne concluded that it is this content—the inappropriate self-disclosure—which determined the other’s reaction, and accounts for the global ratings of interpersonal inadequacy. Two further studies while finding broadly similar results, add some important information. Hammen and Peters (1978) pointed out that Coyne had only used female subjects and targets. They used both males and females in the role either of interviewer or interviewee, with the interviewee taking the role of a depressed or non-depressed person in five-minute telephone conversations. They replicated Coyne’s finding of mood disturbance in interviewers after talking to a ‘depressed’ person, and of more rejection of ‘depressed’ people by the interviewers. But the predominant finding was that opposite-sex ‘depressed’ individuals were rejected far more than were samesex ‘depressed’ people. Furthermore, by having interviewees play roles, the content of the interview could be controlled in this experiment. Specifically, there was no more personal information divulged by ‘depressed’ than by ‘non-depressed’ role-players, so that Coyne’s speculation that overexposure of one’s own life problems might be responsible for alienating the other person seemed not to explain these results. The ‘depressed’ interviewees mentioned


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the same range of problems, but, unlike ‘non-depressed’ interviewees, blamed themselves and expressed hopelessness about the eventual resolution of the problems. Wortman et al. (1976) have in fact found that such disclosure of a personal problem with blame attributed to the self elicits more negative reactions than if external circumstances are blamed. Howes and Hokanson (1979) asked thirty male and thirty female undergraduates to interact with a ‘depressed’, ‘non-depressed’, or ‘physically ill’ confederate for seven minutes while waiting for an experiment to begin. Although subsequently the subjects rated the ‘ill’ confederate as ‘functionally impaired’ to the same extent as the ‘depressed’ confederate, they significantly more often rejected the ‘depressed’ individual. This rejection was not, however, correlated with mood disturbance, levels of which did not vary with the type of confederate with whom subjects were interacting. These three experiments taken together provide strong evidence that depressed individuals alienate those with whom they interact; that this alienation is stronger for opposite sex interactions; that part of the effect may be mediated by the affect induced in the non-depressed partner, and that it seems to be the mentioning of personal problems with self-blameful and hopeless statements attached which causes both the mood disturbance and the alienation in the non-depressed recipient. Interestingly, the fact that two out of the three studies used telephone interactions demonstrates that deficiencies in observable non-verbal communication, such as eye contact and posture, are not necessary for such alienation to occur.

ASSERTIVENESS AND MOOD: WHICH COMES FIRST? In evaluating the earlier behavioural formulations, I remarked that correlations between depression and the behavioural variable of interest (e.g. pleasant activities) was not sufficient to say which came first. Sanchez and Lewinsohn (1980) have attempted to address the issue of causal primacy between depressed mood and assertive behaviour. Each variable was rated on a daily basis by twelve patients over a five-week period. In addition to computing the same day correlation between the two variables (which turned out to be -0.5) they could also compute the cross-lagged correlations for each subject. That is, they computed the correlations between any day’s assertion rating and the day before’s and day after’s mood rating. They found that the averaged correlation for their twelve subjects, between any day’s depressed mood and next day’s amount of assertive behaviour, was -0.017 and not significant. The correlation between any day’s assertive behaviour and the next day’s mood was 0.5, and significant. They conclude that their results ‘suggest that rate of emitted assertive behaviour may indeed be better able to predict subsequent level of depression than level of depression can predict subsequent rate of emitted assertive behaviour’ (p. 120). This conclusion is somewhat premature. Firstly, the choice

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of computing correlations with a lag of one day is quite arbitrary. It is very likely that interactions between mood and behaviour are quite complex— certainly complex enough to justify experimenting with lag 2 or lag 3 to assess this complexity. Secondly, they make no mention of how the autocorrelations were derived for each subject. It seems that they did not make allowances for the statistical dependence of scores for one day on scores of the same variable for previous days. Thirdly, none of the statistical assumptions underlying the use of cross-lagged correlation analysis appears to have been met (Kenny, 1975; Cook and Campbell, 1979). Finally, and most damaging to their conclusions, they draw conclusions about the difference between two correlations on the basis that one is statistically significant and the other is not. That is invalid. They should have tested the specific hypothesis that there was no difference between the correlations. In fact, when the difference between these correlations is computed, the t-test value is 0.81 which is not significant. These data do not therefore allow the conclusion that one variable predicts the other in one direction better than the reverse. However, the results remain very suggestive, and provide better evidence than most theories have done for the relevance of assertive behaviour in maintaining depression. Taken together with the evidence that depressed people alienate others, the evidence cited above suggests that downswings in mood may often follow attempts at engaging in interpersonal relationships. These attempts may have gone wrong not because of lack of social skills, but because of what the depressed person has wanted to talk about. Inappropriate disclosure may make the social situation genuinely more difficult for them. Once the other person has been alienated, it may take better social skills than most people have to rescue the situation. Thus, it may not be that depressed people have poor social skills. It may be rather that they find themselves (because of what they talk about) more often in social situations which would exceed most people’s capacities. It is hardly surprising that they withdraw altogether from such situations. If this is the case, the important thing for therapy to tackle is not social skills, but the person’s negative and self-blameful way of talking to others. I turn now to a model of depression which focuses more on attitude to the self. In it, self-blame (or lack of self-reward) is seen as one of three problems in attitudes to the self (the other two being self-monitoring and self-evaluation).

SELF-CONTROL THEORY OF DEPRESSION This model emphasizes problems that depressed people have in giving themselves sufficient reward. Rehm (1977) developed Kanfer’s (1970) selfregulation model which divided the control that an individual has over their own behaviour into three stages: self-monitoring, self-evaluation and selfreinforcement. These processes may be illustrated by way of the paradigmatic


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‘self-control’ experiment. In it, an individual performs a task (e.g. attempting to recognize which of three nonsense syllables in an array has occurred in a prior list). Following their choice, subjects can be asked to monitor their success or failure rate, to evaluate their level of success relative to subjective standards of accuracy, and then to give themselves a reward in proportion to how deserving they think they are. Using such techniques, it has been found (Bellack and Schwartz, 1976) that self-evaluation and reinforcement do not necessarily correlate with actual accuracy. In two such experiments subjects were given verbal recognition tests consisting of thirty nonsense syllables, presented on slides, one at a time (one second each). Following a brief rest period, subjects saw thirty slides with three nonsense syllables on each. Their task was to identify the syllable they had seen before. Each set of three was presented for five seconds. College students usually have a 50–60 per cent recognition accuracy on this sort of task. Subjects evaluated each response (on a 0–10 scale in one experiment) and administered reward to themselves by pressing a button which lit up an orange lamp. No feedback about a subject’s accuracy was provided. The results were clear. There was no correlation either between actual performance and subject’s evaluation of their performance, or between their actual performance and the amount of reward that they gave to themselves. The maximum number of self-rewards was thirty. Subjects varied between zero and twenty, but those who gave themselves low ratings and low numbers of self-reward had done no worse on the task than those who gave themselves a large amount of self-rewards and evaluated their performance highly. Clearly large individual differences in self-evaluation and self-reward styles exist for this task. How much more variance would there be outside the tight control of the experimental laboratory? Such experiments have made it clear that self-monitoring involves more than the passive registration of stimuli in the environment (Rehm, 1977). Rather it is an active scanning which selectively perceives and encodes into memory. Whereas non-depressed individuals perform this function appropriately, depressed individuals are hypothesized to attend selectively to negative aspects of themselves and their world. Self-evaluation is performed on the basis of criteria that are set too high to achieve, so that overt and covert rewards are rarely awarded. Thus the basis for normal rates of behaviour (self-regulation) in the relative absence of external control is diminished, and the depressed individual’s behavioural repertoire is disrupted. In further statements of the self-regulation model, Kanfer and Hagerman (1981) amplify the distinction between the monitoring of one’s own behaviour and evaluation of it according to current criteria. These criteria may be shortor long-term. Short-term criteria usually centre around performance or behaviour which is relevant only to the immediate situation of specific limited goals (e.g. stumbling when running to catch a bus may mean nothing more than a grazed knee and a ten-minute delay in getting to the office that

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morning). Long-term criteria, however, often relate to maintenance of enduring personal goals (e.g. stumbling when running in the athletic trials to determine who represents your country in the Olympics). In these examples, the situation clearly predefines the criteria which can be used to judge the significance of the same event (stumbling), but most situations are not so clear-cut. Failing to see quickly what you require in a supermarket is a common event, which, if thought about at all, may cause a non-depressed person to conclude that they are not ‘on form’ that day. A depressed person may conclude that they are dementing, because they will see it in the context of other similar events over a long time period. So it may be extremely important whether long-term or short-term standards are accessed in response to ambiguous situations. Accessing the wrong criteria for self-evaluation leads to poor or absent selfreinforcement and increased self-punishment. Evidence consistent with Rehm’s 1977 formulation has taken the form of results showing that depressed and non-depressed subjects do indeed differentially reward and punish themselves as predicted by the theory (Rozensky et al., 1977; Lobitz and Post, 1979). The theory has also led to several successful treatment studies (e.g. Fuchs and Rehm, 1977; Rehm et al., 1979), which although not reviewed in Chapter Four because they used a group rather than individualized approach, have found that an approach which combines self-reinforcement, thought monitoring and evaluation and activity monitoring can be very helpful.

LEARNED HELPLESSNESS AND DEPRESSION Social skills and self-control theories emphasize the adequacy or inadequacy of rewards provided by other people or by oneself. By contrast, in learned helplessness theory, Seligman and his colleagues came to emphasize not the adequacy of reinforcement, but the contingency between actions and reinforcement. In 1967, Overmier and Seligman, in the course of investigating the effects of Pavlovian fear conditioning had found that dogs given inescapable and unavoidable stressors in one situation (the Pavlovian Hammock) later failed to learn to escape or avoid a similar stressor in another situation (the shuttlebox). Further research found similar phenomena in cats, fish, rats, mice, birds, primates as well as man. Maier and Seligman (1976) outlined three outcomes of exposure to uncontrollable aversive events: 1. Motivational deficits: Animals that had been exposed to inescapable stress did not subsequently initiate escape responses in the presence of such stress. 2. Cognitive deficits: Animals that had been exposed to inescapable stress were slower to learn that their responses could control future stresses; i.e.


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if the animal made a response that produced relief, it had trouble ‘catching on’ to the response-relief contingency (Seligman, 1974). In humans, this effect of uncontrollability had been shown by assessing the number of trials taken for a subject to ‘catch on’ to the pattern underlying a series of anagrams. Subjects given prior exposure either to inescapable noise or insoluble discrimination problems took longer to perceive the pattern (Hiroto and Seligman, 1975; Miller and Seligman, 1975). 3. Emotional changes: Maier and Seligman presented data from a number of sources to support the claim that inescapable trauma had emotional effects: there was evidence that following only one such trauma in dogs, subsequent helplessness deficits dissipated over forty-eight hours, which they suggested hinted at a transient emotional (hormonal) effect; human subjects who performed tasks while being shocked but were not allowed to take time-outs when they wished, had been found to show consistently higher blood pressure than subjects who were allowed to specify when they wished to take time-outs (Hockanson et al., 1971). The hypothesis proposed by Seligman and co-workers to account for these phenomena was ‘learned helplessness’ (Seligman, 1974, 1975). It assumed that organisms could learn not only about the contingencies between instrumental responses and the outcomes of those responses but also could weigh up the probability of their behaviour resulting in a specific outcome. When the probability of reinforcement, given a specific response, does not differ from the probability of reinforcement in the absence of that response, responding and reinforcement are independent, i.e. the organism has no control over outcomes. The learned helplessness hypothesis argued that motivational and cognitive deficits and emotional changes follow when an organism has learned that responding and outcome are independent. The motivational deficits follow inescapable stress because part of the incentive for making such responses is the expectation that they will bring relief. The cognitive deficits follow inescapable stress because, having acquired a cognitive set in which responses are irrelevant to outcomes, it will be harder to learn that responses control outcomes when they actually do. The presence of emotional changes did not follow directly from the helplessness hypothesis, but Seligman cited evidence that exposure to uncontrollable trauma produced more conditional fear, ulcers, weight loss and defecation in animals, than controllable stress. However, it was the suggestion that this learned helplessness phenomenon could be a model of reactive depression in humans which gave the greatest impetus to research, particularly in the attempts to find human analogues of the animal work. Just as animals exposed to inescapable stress showed later motivational, cognitive and emotional changes which undermined effective instrumental responding, so reactive depression may have resulted from stress perceived as uncontrollable which would lead to the expectation that future

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reinforcements would be out of the person’s control. This expectation was hypothesized to lead to the passivity of depression (motivational), the negative expectations of depression (cognitive) and the affective disturbance in depression (emotional). A great deal happened in the few years after publication of Seligman’s book on helplessness (1975). For example, it soon became clear that many of the human laboratory helplessness demonstrations did not require a ‘learned helplessness’ model to explain them (Coyne et al., 1980; Williams and Teasdale, 1982). Coyne et al. referred to the similarity between helplessness phenomena and the large number of studies using similar procedures (to similar effect) in the test anxiety and achievement motivation literature. They surmised that if laboratory helplessness phenomena were anxiety-based, they ought to be alleviated with ‘pleasant relaxing imagery’ inserted between pretreatment and test phases. They indeed found that instructing subjects to imagine a pleasant mountain scene ‘in order to relax you’ prevented deficits on twenty patterned anagrams following uncontrollable noise pretreatment. Williams and Teasdale (1982) found evidence that behavioural deficits on laboratory tasks used in helplessness research could be reproduced in subjects who had a low expectancy of success on a task thought to be of low importance, and in subjects who had a low expectancy for an important task who then met initial difficulty performing that task. Explanations of these results were proposed in terms of four variables: expectancy of success, motivation to succeed, amount of effort required and the cost of effort. No explanation in terms of perceived or expected non-contingency between action and outcome was necessary. Alternative explanations for helplessness deficits have continued to appear. In one such recent study Mikulincer (1989) proposed that learned helplessness deficits were due to ‘off-task cognitions’. Subject’s proneness to cognitive interference was assessed prior to being given failure or no failure feedback in the first phase of an experiment. The subsequent test task used to assess helplessness varied in its memory load. Consistent with the hypothesis, only subjects defined as vulnerable to cognitive interference showed helplessness, and then only on the high memory load test task. Furthermore, accuracy on the test task was associated with the frequency of reported off-task cognitions. Once again, no explanation in terms of non-contingency between action and outcome was necessary. However, the most significant development in learned helplessness theory has come, not from outside the helplessness camp but from within it. At about the same time as Seligman’s landmark book, Helplessness, was published and certainly by the time the large review paper on ‘Learned helplessness’ by Maier and Seligman (1976) appeared in print the theory was being substantially modified. A draft paper was even then circulating between London, Pennsylvania and Oxford. A number of doubts about the robustness of the model had occurred simultaneously to Seligman himself (on sabbatical


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in London in the mid-1970s), to Lyn Abramson in Pennsylvania, and John Teasdale in Oxford. Their important paper in 1978 (Abramson, Seligman and Teasdale) represented a ‘reformulation’ of learned helplessness as applied to humans, in attributional theory terms. I shall start the next chapter, which will focus on cognitive accounts of depression, by examining this attributional reformulation.

Chapter 3

Psychological models of depression II The cognitive foreground

When psychologists refer to cognitive models of depression, they are usually referring to one of two theories—that of Aaron Beck, who has been writing about the influence of thoughts, images, attitudes, and schemas on mood since at least the early 1960s (see Beck, 1964); and that of Martin Seligman, whose theory of learned helplessness I reviewed in the previous chapter. Seligman’s theory differed from that of Beck in that it grew out of laboratory research with animals. It was nevertheless a ‘cognitive theory’ in the sense that the animal or human was presumed to be computing and comparing two probabilities (or expectations) of outcomes given a response versus the absence of a response. By contrast, Beck’s model grew out of observation of the thoughts, images and dreams of depressed patients. It made use of concepts from the rapidly expanding field of information processing (most notably the concept of the schema) and quickly became the framework within which a structured psychotherapy developed. Originally, the links between these two cognitive theories were very tenuous, because of their different origins (see Seligman, 1981 for his description of similarities and differences). When the original learned helplessness account ran into difficulties, it was reformulated in terms which took into account a variable (attribution) which was very similar to the notion of dysfunctional attitude developed by Beck (1976). But it was a much more tightly formulated notion than dysfunctional attitudes, since it was able to benefit from several years of careful research into attributional processes (see Weiner, 1986). As such, the attributional formulation led to a large number of studies examining correlational and longitudinal relationships between attribution and depression. Because the attributional theory grew out of the helplessness framework reviewed in the previous chapter, I shall review it before reviewing that of Beck.

THE ATTRIBUTIONAL REFORMULATION OF DEPRESSION A summary of the main proposals of the attributional reformulation was given by Seligman in a 1981 paper. The new model had four premises, the 26

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co-occurrence of which was hypothesized to be sufficient for depression to occur: 1. The individual expects that a highly aversive state of affairs is likely (or a highly desired state of affairs is unlikely). 2. The individual expects that he will be able to do nothing about the likelihood of these states of affairs. 3. The individual possesses a maladaptive attributional style so that negative events tend to be attributed to internal, stable and global causes, and positive events to external, unstable and specific causes. 4. The greater the certainty of the expected aversive state of affairs and the expected uncontrollability, the greater the strength of motivational and cognitive deficits. The greater the importance to the individual of the uncontrollable event, the greater will be the affective and self-esteem disruption. For a reason which is not entirely clear, most subsequent interest has focused on the third premise, that maladaptive attributional style predisposes the individual to react in a depressive way to the presence of aversive events or non-occurrence of positive events. This component of the model states that attribution for an uncontrollable event determines the individual’s response to that event. For example, if an exam was failed you might say to yourself either that you failed because you didn’t have the necessary ability or because you didn’t try hard enough (both internal attributions). Note however that ability is a rather more unchanging or ‘stable’ cause for your failure than effort. Effort may be increased the next time the exam comes around whereas ability is seen as rather less changeable. Or you may say that you failed because the exams set by that examination board are always very difficult (another ‘stable’, but this time ‘external’ attribution) or that it was just bad luck and next time may be OK (‘unstable’ and ‘external’). Table 3.1 shows these four possible attributions and their categories. These attributions may also be either global or specific. You may say you hadn’t the ability either specifically, because it was, for example, a statistics exam which for you correlates with no other exam performance, or globally, because you are just no good at taking formal exams and don’t understand anything on any of your college courses anyway. Clearly one would expect differences in attributions such as these to make a large difference in the Table 3.1 Possible attributions for failing an exam

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behavioural and affective impact of the original event. The theory proposes that negative events attributed to internal (personal), stable (unchanging) and global (wide-ranging) attributions will be more devastating emotionally. In particular, internal attributions for failure (and external ones for success) tend to lower self-esteem; stable attributions for failure (and unstable ones for success) tend to produce long-lasting deficits; and global attributions for failure (and specific ones for success) produce depressive deficits which generalize to many situations. Note that this attributional component of the model is only one of four premises. Early research neglected the other premises, for example the first and second premises that an event perceived as uncontrollable is deemed a necessary co-occurrence of the other premises for depression to occur. That is not to say that depression cannot occur by other means (biological, prolonged anxiety or heavy workload, etc.), but that on this theory, all four premises are necessary. A detailed discussion of these aspects of the model will be found in Chapter Ten. The researchers who have looked at the attributional component of depression have found ambiguous results. Some of these are detailed in Chapter Ten, but it is appropriate here to mention some studies which have examined these variables in some depth. Hargreaves (1985) examined fifty depressed patients (divided equally between the sexes) who had been referred to psychiatrists or psychologists for management of depression. The sample included inpatients, outpatients, daypatients and general practitioner patients. All were between the ages of sixteen and sixty-five years, with no psychoticism, mental deficiency or organicity, and no history of alcohol problems or drug addiction. All had a Beck Depression Inventory (BDI) score of at least 15. Control subjects, matched for age and sex (twenty-five males and twentyfive females) were recruited from a subject panel. Depressed and control subjects completed the Beck Depression Inventory; the Attributional Style Questionnaire (which gives a score of an individual’s tendency to see positive and negative events as caused by internal, stable or global factors, as well as a rating of the importance of the outcome) (Seligman et al., 1979); the Locus of Control Scale (Rotter, 1966); a Self-Esteem Questionnaire (Rosenberg, 1965); and the Eysenck Personality Questionnaire (Eysenck and Eysenck, 1975). Thus it was possible not only to see if depressed patients were characterized by any particular attributional style, but also to examine the personality correlates of attributional style. In answer to the first question, no differences in attributional style were found between the depressed and control groups. Furthermore, when the correlates of attributional style on Seligman’s questionnaire were observed, they were disappointing. For example, there was no significant correlation in the depressed group between Seligman’s internality scale and the Rotter Locus of Control internal-external score (r=-0.252 and -0.003 for internal attribution to success and failure respectively). For non-depressed subjects these

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correlations were r=-0.414 (p14 and unipolar, nonpsychotic major depressive disorder on the RDC). All were aged between twenty and sixty. All groups improved significantly. Despite a tendency for more of the CBT and CBT+TCA to achieve remission than the TCA alone group (on the basis of Hamilton score of 6 or less plus two out of three selfreport measures of improvement: 57 per cent, 65 per cent and 38 per cent of the CBT, combination, and TCA alone group respectively) these differences were not statistically reliable. Patients were followed up at three, six and twelve months. The proportion of patients requiring medication during this twelve-month period was 20 per cent, 42 per cent and 50 per cent in the CBT, CBT+TCA combination, and TCA alone groups respectively. The equivalent proportion of patients needing

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further psychotherapy was 19 per cent, 30 per cent and 51 per cent. The suggestion that cognitive therapy might have effects beyond the acute treatment is one to which I shall return after considering the last major study of the 1980s—the NIMH multicentre trial. Elkin, Shea, Watkins, Imber, Sotsky, Collins, Glass, Pilkonis, Leber, Docherty, Fiester and Parloff (1989) Up until now, I have been reviewing studies which, though starting with behavioural treatments in the early 1970s, gradually focused more and more on cognitive-behavioural treatment of Beck. Other developments had been occurring in psychological treatments, which are beyond the scope of our review simply because this book is concerned with individual behavioural and cognitive treatment. As Beck et al. acknowledged, cognitive therapy was not the only psychological treatment which appeared to be effective in treating depression: those approaches that combine both cognitive and behavioural procedures (e.g. Rehm’s self-control or McLean’s behavioural-cognitive marital skills training) along with cognitive therapy and the newly refined interpersonal psychotherapy (IPT) seem to be the most efficacious psychotherapy interventions for depression…. Yet another report by Bellack et al. (1981) presented further evidence of the relative efficacy of structured psychological intervention in comparison to standard antidepressant drugs. (Beck et al., 1985:147) This last comment was a reference to the use of social skills training, and meant that at least five types of psychotherapy were considered effective. Beck et al. (1985) concluded that ‘the type of psychotherapy may not prove to be nearly so important as the extent to which it is adapted to a specific symptomatic focus’ (p. 147). In 1989 Elkin et al.’s multicentre trial found results which reinforced this conclusion. Two hundred and fifty patients at three sites were randomly allocated to receive Beckian cognitive therapy, interpersonal psychotherapy (IPT, Klerman et al., 1984), imipramine plus clinical management (CM) or placebo plus CM. To be included in the trial, patients had to be unipolar, non-psychotic, outpatients (Research Diagnostic Criteria, major depressive disorder), who had a score of at least 14 on the Hamilton Depression Scale. The usual exclusion criteria (bipolar, alcoholism, etc.) operated. The tricyclic used was imipramine (a mean of 185 mg/d with 95 per cent of patients having at least 150 mg/d). Careful guidelines were laid down, not only for the CBT and IPT therapy, but also the CM. Experienced psychiatrists conducted these twenty to thirty-minute weekly interviews (after an initial session of fortyfive to sixty minutes). The guidelines for CM specified discussion of medication

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and side-effects, plus a review of patient’s clinical status and provision of support, encouragement and direct advice if necessary. All treatments were planned to be sixteen weeks in length, with a range of sixteen to twenty sessions. The mean number of sessions for patients who completed treatment turned out to be 16.2. Each psychotherapy session lasted fifty minutes. The proportion of patients dropping out of various treatments was not significantly different between the groups: 32 per cent for CBT, 23 per cent for IPT, 33 per cent for TCA+CM and 40 per cent for placebo+CM. All treatments made significant gains, though there was a treatment×site interaction for the more depressed/impaired patients (Global Assessment Scale score = 50), such that IPT did very well on one site, CBT on another, with TCA+CM being more consistent throughout sites. The similarity of outcome of the four treatments was shown by the fact that of twelve primary statistical analyses, only four revealed any statistically significant results. Two of these were analyses of those patients who completed treatment (N= 155 in the analysis, though 162 had completed, data not having been obtained for seven subjects). These significant findings concerned the Hopkins Symptom Checklist 90 and the Global Assessment Scale (GAS) and showed tricyclics to be superior to placebo. No other comparison was significant. The two other significant effects were found in their analysis of all patients who had entered treatment (N=239) even if they had dropped out immediately and were found on the Hamilton and the GAS. Post-hoc tests, however, showed that only on the GAS could any between-group difference be detected; again a significant difference between the TCA+CM group and placebo+CM group. Looking at the final scores (for completers) on the BDI (see Table 4.4) one can see why the analyses yielded so few differences. Outcome for all treatments (including the placebo+CM) was very similar. A slightly different picture emerged from two supplementary analyses. The first examined the proportion in each group that achieved remission (a score of 6 or less on the Hamilton Rating Scale). These are shown in Table 4.3 for the completers (N=155) and the total sample (N=239) mentioned above. The pattern shown in Table 4.3 is for the three active therapies (TCA +CM, IPT, and CBT) to achieve generally higher proportion of remission Table 4.3 Proportion of patients in remission at end of treatment (Elkin et al., 1989)

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than placebo, and not different from each other. However, the IPT and TCA +CM were sufficiently higher than the placebo+CM to achieve statistical significance. The second supplementary analysis divided the sample into high and low severity (=20 on the Hamilton; =50 on the GAS). For the less severe patients, the outcome for all four groups was indistinguishable. For the more severe patients there was a clear advantage for TCA+CM, placebo was worst with the two psychotherapies in between and not differing from each other. Once again, the TCA+CM and IPT groups, though not differing from CBT, were sufficiently different from placebo to achieve significance. In none of these supplementary analyses did cognitive therapy differ significantly from placebo+CM. Consistent with the conclusion emerging from the studies we have reviewed, whether one looks at completers or at the total sample in Elkin et al.’s study there was no evidence of a significant difference between the three active treatments. Elkin et al. themselves conclude: ‘in the major analyses in this study, there was no evidence that either of the psychotherapies was significantly less (or more) effective than imipramine+CM’ (p. 977). And regarding the comparison between IPT and CBT: there is no evidence in this study of the greater effectiveness of one of the psychotherapies on measures of depressive symptoms and overall functioning (although…there was adequate power in the primary analyses for detecting any large effect size differences that might exist). (Elkin et al., 1989:979) Although there was limited evidence of the specific effectiveness of IPT and no evidence of the specific effectiveness of CBT when compared to placebo +CM the authors discuss these findings in the light of the more surprising conclusion that there was only some, but not a great deal of evidence of the superiority of imipramine+CM over placebo+CM. The fact that only four out of the twelve primary analyses yielded significance was very puzzling given that it included a straight comparison of active antidepressants against an inactive placebo. Final assessment of each of these therapies must await the results of the follow-up study, some of which are described below and present a somewhat different picture, with cognitive therapy being most effective in the longer term. Returning to the acute treatment trial, examination of the percentage change scores on the BDI (Table 4.4) shows that the three active treatments achieved levels of improvement broadly comparable with previous studies (with TCA+CM doing better than any previous study of TCA alone—presumably due to the carefully described and supervised clinical management component). What is striking is that the placebo+CM group did as well as active treatments have in previous studies. Elkin et al. also noted the fact that their placebo, for


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some reason, exceeded the performance of placebos in standard drug trials presumably due, once again, to the clinical management. If we had become accustomed to finding that different active treatments produced similar outcomes (Taylor and Marshall, 1977; Zeiss et al., 1979; Murphy et al., 1984) it was unexpected that a placebo condition should do so well. This was most surprising for patients with a Hamilton score of less than 20, where there was no advantage at all for tricyclics or for the psychotherapies over the placebo+CM (though it is important to note that placebo did not do so well for the more severe subsample). This result potentially threatens both advocates of drug treatment and advocates of psychotherapy for less severely depressed patients. Further work is therefore needed to understand what the therapeutic property of the placebo+CM treatment was. Clearly something is happening here. Is it increased optimism in the patients? Or increased courage to try and do things that they have been avoiding doing, due either to the pill or to the advice? The theory on which interpersonal psychotherapy is premised would predict that what was happening was that somehow, this clinical management was allowing the patient to get over grief, to handle role transitions, to resolve interpersonal disputes and to make up for interpersonal deficits. The theory on which cognitive therapy is premised would suggest that these patients recovered because they were gaining distance from their negative thoughts, engaging in activities to gain a sense of mastery and pleasure, and thereby being enabled to challenge their dysfunctional attitudes towards themselves. Returning to the parable of the mineshaft (Chapter One), these may have been people who were predominantly active problem-solvers who simply needed encouragement to use the skills that depression had temporarily undermined. My guess is that all of these things were happening: interpersonal, cognitive and behavioural changes. In the less severe patients, such changes were more easily prompted. The findings for the more severe patients are less clear-cut. There were consistent treatment×site interactions for these patients. At one site, cognitive therapy did extremely well, producing results comparable with imipramine. At another, IPT did well in a similar way. Only further examination of the data will reveal whether it was patient, therapist or situational characteristics which were the cause of this pattern of results.

SUMMARY OF THOSE STUDIES WHICH USE THE BECK DEPRESSION INVENTORY Table 4.4 shows those of the studies which have used the BDI to evaluate a package of treatments including both cognitive and behavioural components, thus enabling some interesting (if crude) comparison from study to study. Several conclusions emerge from scrutiny of these data. Firstly cognitivebehavioural therapy is efficacious with a variety of populations of depressives—clinical and subclinical, from a fairly wide range of social class,

1. Teasdale et al.’s CBT group also received Treatment as usual which often included TCAs

Table 4.4 Percentage change scores on Beck Depression Inventory (for inpatient studies see Ch 8)


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in both the Americas, Australia and Europe at least. Secondly, the combination of drugs and CBT is sometimes more efficacious than CBT alone; CBT alone is sometimes more efficacious than drugs alone; but drugs alone have not so far been found to be superior to CBT. Thirdly, the inclusion by at least one study (McLean and Hakstian) of two alternative psychological techniques each plausible in its theoretical basis, and with one (relaxation) involving homework assignments and the other (psychotherapy) practised by therapists for whom this approach was preferred, strongly suggests that the superiority of CBT when it occurs is not a function of non-specifically raised efficacy expectations. Focusing on outpatients, the mean percentage change across the six samples of outpatients who have received cognitive-behaviour therapy alone is 65.7. This compares with a mean of 63 per cent in the five samples of outpatients receiving TCA alone (including Elkin et al.’s TCA+CM group), and 72 per cent for the three samples of outpatients which have received a combination of tricyclics and cognitive therapy.

FOR WHOM IS COGNITIVE-BEHAVIOURAL THERAPY MOST SUITABLE? Research so far has not established its usefulness with bipolar depressives, highly regressed patients, or patients with delusions or hallucinations (‘psychotic’), but that is because the research has not been done, rather than because any studies have actually demonstrated its inefficacy. Endogeneity or chronicity seem not to predict outcome (Kovacs et al., 1981; Blackburn et al., 1981; Beck et al., 1985). Personality characteristics seem equally irrelevant; neither McLean and Hakstian (1979) nor Kovacs et al. (1981) found that Eysenck’s scales correlated with outcome. McLean and Hakstian’s study of 178 primary depressives remains the most comprehensive study of predictive variables. A large number of variables were assessed including sociodemographic variables, number of recent life events, personality (EPI), number of social contacts, cognitive depression—negative thoughts, indecisiveness, poor memory, severity of depression, episode duration, employment status, as well as measures of coping ability. Four distinct groups emerged from a cluster analysis but none did any better with any of their treatment conditions than any other. A similar result has been reported by Shea et al. (1990). Although patients in their trial (NIMH) had a worse outcome on social functioning if they had a personality disorder, the type of personality disorder did not affect the outcome. Some analyses have been done of response to treatment in general (i.e. including both drug and CBT groups). Blackburn et al. (1981) analysed the characteristics of those who did not complete treatment in their study. They were found to be significantly more severely depressed (higher BDI and HRS(D)), more irritable, more negative and less educated than completers, but none of these variables differentiated drug from CBT dropouts. Of those

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who completed, the worst outcome occurred for those with the longer duration of the current episode. By contrast, no variables at all (demographic characteristics, history of illness factors, pretreatment clinical or self-rating depression scales) could be found by Rush et al. which differentiated the patients who dropped out of their trial from those who completed the trial. On the other hand analyses of those who had the worst outcome by Hollon (cited in Fennell and Teasdale, 1982) found that four or more of the following predicted a worse outcome: 1. 2. 3. 4. 5. 6. 7.

Beck Depression Inventory score ≥30 duration of current episode ≥6 months inadequate response to previous treatments ≥2 previous episodes associated psychopathology overall impairment as rated by clinicians (moderate or severe) poor estimated tolerance for life stress

However these patients also did worse in response to antidepressant medication. When twelve-month follow-up assessments of those who did complete treatment were made, depression severity at that time was not predicted by history of illness, sociodemographic variables or pretreatment BDI score. The only predictive variables were patient age (BDI vs age: r= 0.29; p7. Of the twenty-six patients who recovered during the treatment phase, seven (27 per cent) relapsed. Three of these had received standard treatment (out of six ‘recovered’=50 per cent) and four had received combination treatment (out of 20 ‘recovered’= 20 per cent). The most striking finding was the overall treatment response. When all patients who entered treatment were considered, a significantly higher percentage of patients given additional CBT achieved remission (i.e. recovered and stayed well): 54 per cent vs 18 per cent for the standard pharmacotherapy group. (The percentages for those thirty-one who completed treatment are 68 per cent and 33 per cent for combination and standard treatments respectively.) Although the numbers in this study were small, as for most inpatient studies

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to date, the fact that the results were comparable to outpatient treatment and follow-up studies (see Chapter Four) suggests that the results are reliable. Finally, Bowers (1990) conducted a controlled trial in which TCA alone (nortriptyline; initial dose range 25–75 mg/d; the dosage rising to 100–200 mg/d) was compared with the same dose of TCA combined either with CBT or with relaxation. There were ten inpatients (age eighteen to sixty years) (DSM III unipolar depressives) in each group. The psychotherapy was conducted daily for twelve days. The mean number of days in hospital was 31.9 days for the TCA alone group, 29.4 for the CBT+TCA group and 27 days for the relaxation plus TCA group. Independently rated Hamilton Rating Scale for Depression scores shifted from 22.1 to 8.5, 20.7 to 6.6 and 16.5 to 7.3 in the TCA alone, TCA plus CBT and TCA plus relaxation respectively. The corresponding Beck scores were 31.2 to 19.6 (37 per cent); 24.2 to 10.1 (58 per cent) and 25.8 to 9.3 (64 per cent) respectively. These results were very encouraging for the addition of psychological treatment to the TCA. Even more encouraging was the analysis of the proportion in each group who achieved the criterion of ‘remission’ (Hamilton score of 6 or less). Whereas eight out of ten patients in the TCA+CBT group had a score of 6 or less, only one out of ten of the TCA+relaxation group and only two out of ten of the TCA alone group achieved remission. These studies suggest that a range of behavioural and cognitive procedures, applied systematically, may have a significant effect in combination with antidepressants. No study has yet compared psychological treatment alone and in combination with antidepressants, with antidepressants alone. However, the evidence from clinical trials with outpatients (reviewed in Chapter Four) suggested that the combination of psychological and drug treatments has never been found to be less effective than either alone. So although we await controlled trials to examine this specific question, there appears no reason to stop one treatment while the other proceeds, except for the evident advantages of giving patients who may have been on psychotropic medication for a long time a chance to come off their drugs in the protected environment of an inpatient unit and while alternative psychological treatments are available. It is to a more detailed description of these alternative psychological treatments that we now turn.

OVERVIEW OF TECHNIQUES When the cognitive therapy package was introduced earlier (Chapter Six) I pointed out how, for the more severely depressed patients at the outset of therapy, it was more appropriate to focus on behavioural targets using behavioural techniques, rather than on cognitive aspects. Behavioural approaches are often criticized for being too objective and unfeeling, for not taking into account the personal experience of the client. But in some contexts,

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this may be its strength. After a long period of depression and after many periods in hospital, the patient, their family, the therapists and staff find it difficult to be objective about the situation. Because behavioural approaches so clearly try to stand outside personal experience, it may lay essential foundations on which relationships and self-esteem may be rebuilt. Patients, staff and family members who have agreed simply to count the number of times a certain objective ‘behaviour’ occurs, can find this a very liberating experience. Consistently defining these behaviours as the central aspect of depression to be changed encourages all concerned to see things more clearly. There is a greater chance that all involved will be able to agree on what changes need to be made. The irony is that ignoring personal experience may sometimes be the best way to change it. This section gives information about techniques that have been used successfully with people who are more severely and more chronically depressed. Generally, the number of sessions is greater than conventional cognitive therapy, though the total number of weeks in therapy may not be longer. Shorter sessions are held two or three times a week and wherever possible the whole milieu of the unit is used to promote awareness of cognitive and behavioural principles of coping with depression.

CONTINGENCY MANAGEMENT Rationale Depressive behaviours per se constitute the disorder. They can be manipulated by encouraging the performance of positive behaviours (by a token economy or contingency management scheme) which are incompatible with symptomatic manifestation. Aims of treatment The aim is to increase frequency of ‘work behaviour’, coping strategies and interpersonal efficiency which will be incompatible with depressive behaviour. Procedure Because the treatment is usually carried out in an inpatient or daypatient setting, staff can observe and interact with patients over a long period each day. Many of a patient’s ‘daily-living’ activities, such as cooking, cleaning, personal hygiene and social interaction, can be made the focus of treatment. Typically, the patient consents to participate in a scheme which is running for a whole ward or unit. (Some therapists maintain that programmes for individuals within a normal ward are impractical, noncost-effective, and more difficult to control. However,


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there is nothing in principle to stop therapists from adapting these procedures for use with individuals in normal inpatient or daypatient settings.) In introducing the patient to the scheme, a great deal of didactic explanation of its underlying principles is thought to be essential. Some patients and relatives will readily accept the philosophy, others may not. Liberman and Roberts (1976) give the following written information to patients participating in the Coupon Incentive Scheme at their day treatment centre. 1. The emphasis is on active participation in the programme as the ‘best therapy’. 2. A brief description of way the unit is run—meals, recreation, therapy, etc. 3. Introduction to ‘token economy’ concept—tokens given on predetermined basis at a set rate for jobs around unit. 4. Procedure for exchange of tokens (snacks, coffee, recreation, etc.). 5. Procedure for monthly renewal of tokens and ‘fresh start’. 6. Management of token economy by patients themselves chosen by all patients weekly, with staff members in support. 7. Patients are asked to sign a consent form. These details give something of the ‘flavour’ of the coupon incentive scheme, and although not appropriate for many settings, it may be modified for use in other centres. Note that it is explicitly behavioural-educational, but that the patients run many aspects of the scheme themselves. One important aspect of the approach in Liberman and Roberts’ centre, was that the token economy was not the only therapy strategy operating. Each patient was assigned to a therapist (nurse, psychological technician, rehabilitation worker—ten in all) who worked out individual strategies for each patient, including homework assignments. Other activities during the day included workshops (with the emphasis again on education) which taught skills in community living and personal finance, as well as conversational skills, use of public agencies, etc. Example of contingency management in a daypatient setting Liberman and Roberts (1976) describe the case of Sarah Jane, a thirty-yearold married ex-secretary with three children. On admission to their day treatment centre she had a history of loss of interest in everything, ‘feeling like a nothing’, staying in bed for long hours, failure to cope with housework and childcare. On previous admissions to other units she had been described as agitated, tremulous and apathetic. Her diagnosis was ‘neurotic depression’. Psychotherapy had been tried during a previous admission to no avail. Table 8.1 gives a specification of problems and goals for Sarah Jane. The staff at the centre where Sarah Jane was a daypatient were encouraged to ignore her negative self-reference and give social approval for her improved

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Table 8.1 Specification of problems and goals for Sarah Jane

personal appearance (as per specification). The treatment of the excess sleeping and ‘deficient housework’ was carried out by pairing the two in a contingency self-management programme which will be described in a later section. Sarah Jane was taken off the medication she had been taking on admission (doxepin and chlorpromazine) (on the grounds that ‘the scientific literature reveals no clear benefit of medication in neurotic depression’). She and her therapist met daily to review the contents of her daily diary. During these sessions also, the therapist ignored remarks about how difficult her housework duties were, and instead enquired further into the details of Sarah Jane’s accomplishments in her assignments. After one month of this intensive day treatment, conjoint marital therapy (one session per week) was started, though it seems that the patient continued to attend the centre on some days until three or four months later—by which time she was doing a three-day-a-week volunteer job. A three-year follow-up revealed that she and her husband had decided to separate by mutual consent. She was leading an extremely happy and fulfilled life. Comment A number of things are notable about the original contracts that were made. Firstly, many may object that it is sexist. ‘Adaptive’ behaviours seem to be geared to increasing comfort with the housewife and ‘sexually attractive wife’ role. This may be so, though it is very important to achieve a negotiated contract between therapist and patient, with neither side being able to impose


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a philosophy on the other. (In fact, the authors were well aware that the causes of this patient’s depression had much to do with her husband’s behaviour, and arranged for marital therapy to take place.) Secondly, in common with much behaviourist formulation, there is no place for ‘reasons’. ‘Verbalizations about feeling sick’ are to be decreased with, it seems, scant regard for what prompts such talk (e.g. actually feeling sick). On the other hand, the indications are that such contracts are willingly negotiated and in some patients there is relief that the focus of treatment is so observable. No therapist would wish to impose such a programme on an unwilling party. Note also, that in this case the token economy scheme was very much a ‘background’ against which these other treatments were implemented. The coupons were given for helping out around the unit, but the modification of particular depressive behaviours (e.g. unkempt appearance) were individually tailored for each patient This individually specific assessment and treatment formulation differs from other token economy programmes. In that of Hersen et al. (1973), for example, patients were awarded blue index cards contingently upon completion of target behaviours in four categories—personal hygiene, responsibility, occupational therapy attendance and work (all off the ward). These assignments were administered by hospital personnel, nonpsychiatric staff. Even within this more rigid system, however, individuals took responsibility for planning their day each morning during the unit’s ‘banking hours’. The indications are that both practices can work well. It is up to individual practitioners to decide which approach they prefer.

APPLICATION OF PREMACK PRINCIPLE Rationale For people who have been severely depressed for a long time, there often seems to be nothing which is rewarding, nothing which can be used as ‘reinforcement’ in contingency management. The Premack principle (Premack, 1959) states that the ‘occurrence of high frequency behaviour should have reinforcing value for low frequency behaviours’. That is, it starts with the assumption that whatever the patient does most of the time is reinforcing for them and can be used to reinforce behaviours they do least frequently. Aim of technique The aim is to draw up a plan with patient, family and staff (where relevant) to ‘make the occurrence of a high frequency behaviour contingent upon a low frequency behaviour’. That is, to allow the person to do what they normally do most of only if they have done (initially a small amount of) what they do least

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Procedure and examples When therapist controls contingency Lewinsohn et al. (1969) present the case of a twenty-two-year-old divorced male who was in financial difficulties, would ruminate on his marital and other failures, feeling suicidal and ignoring his personal appearance. The first step was to identify high frequency behaviour to be reduced (depressive talk). The next step was to identify low frequency behaviour to be increased and to establish a series of targets which the patient agreed were achievable in principle (talking to tutor, making arrangements to recover from his financial plight, making enquiries into availability of various jobs). The therapist then made available more time to listen to depressive talk (if patient wished to talk) only if some prescribed positive steps were taken between sessions. Each interview began with a report on progress the patient had made. If all targets had been met, a full hour session was made available. If little had been accomplished, the therapist was polite but brief, and ended the session within ten or fifteen minutes, suggesting that the patient return three or four days later. Within a few weeks the patient had made and acted upon many decisions, had found a job and arranged a loan to ease his financial embarrassment. Comment There are several points that deserve comment. Firstly theoretical: given that all behaviours have multiple causes, it is doubtful whether a clear contingency between the high probability behaviour and low probability behaviour was established in this case. Activity scheduling itself has been used clinically without making opportunity for occurrence of depressive talk contingent upon it, and may thus have been the effective component Secondly practical: many therapists would be unwilling (a) to terminate a session prematurely for any reason other than by mutual agreement of both parties; or (b) to let the longer session wander aimlessly, directed only by the patient’s wish to discuss self-critical topics. Nevertheless, for some patients who seem to find therapy sessions an end in themselves, and in whom there is evidence of low motivation to pursue targets because of a fear of termination of therapy, this principle may be applicable. In these cases, it can be made clear to the patient that you want to meet weekly to monitor midweek progress, and that there is no point in meeting for long if no homework has been attempted. When patient applies Premack principle to self In Liberman and Roberts’ treatment of Sarah Jane, they included a self-


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managed Premack technique which the patient operated herself when on leave from the unit. Together, the therapist and patient prepared a notebook for use as a behavioural diary, dividing each page into two columns. One column was headed ‘constructive activity’ (low frequency behaviour which they had decided to try and increase). The other column was for recording the particular depressive high frequency activity they had decided to try and decrease—in Sarah Jane’s case, the time spent lying down during the day (approximately five hours at the outset). The patient was urged to go to bed during the day only after she had completed a predetermined amount of adaptive, constructive activity (e.g. housework, shopping, interactions with children). Sarah Jane herself produced the list of constructive activities which would be subject to this scheme. The idea is that as the frequency of constructive activities increases, they gain their own reinforcing qualities independently of the inappropriate activities. This, it is hoped, will improve mood. Gradually the desire to take to bed will decrease. This is what occurred in the case of Sarah Jane. By the end of seven weeks the ‘time in bed’ earned by the completion of constructive activities consistently exceeded the time in bed actually taken up. Comment The use of the Premack principle in this way seems to avoid the disadvantage of the use of the principle by the therapist. It is self-managed and is therefore easier to make plain to the patient exactly what the purpose of it is. Furthermore, it gives permission for the depressive behaviour to take place. My own impression is that depressed patients have often become very immune to attempts by partners, family and friends to spur them into action. Often partners have tried both positive and negative approaches in attempts to prevent the patient lying down on the bed (for example) for a great part of the day—to no avail. Patients themselves are often extremely frustrated and puzzled by their own lack of energy and listlessness. A therapy which allows any amount of this to happen, so long as some (at first) minimal constructive activity has taken place has a lot to commend it. It is this which makes the technique particularly useful in an inpatient setting. If therapist, nursing staff and patient can agree on what small amount of constructive activity on the ward will ‘buy’ what amount of ‘depressive behaviour’ (e.g. lying in bed), this allows all concerned to reduce the unsystematic and frustrating interactions between staff and patients that otherwise often occur. A variant of the Premack principle is used in coverant conditioning. In this procedure, a list of positive self-descriptions are drawn up by the patient with the therapist’s help. The items are written on cards, and the patient is instructed to read through the list before engaging in a high probability behaviour (e.g. smoking, drinking coffee or tea, using the toilet, etc.). The

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aim is an increase in spontaneous use of such positive verbalizations as a result of these ‘conditioning’ trials, but no attempt to decrease the high probability behaviour itself is implied.

COGNITIVE-BEHAVIOURAL MILIEU THERAPY Rationale and aims Chronic patients take longer to engage in psychological treatment, and their problems are multiple, severe and complex. Psychotherapy must reflect this complexity by (a) being multifacetted; (b) by all members of the clinical team being consistent in reinforcing the behavioural and cognitive approach; and (c) by engaging dose family members as part of the collaborative team alongside staff and patient. Procedure The following outline is based on procedures at the Affective Disorders Unit, Newcastle upon Tyne (Scott, 1988b). Patients are admitted to a specialist unit in which biological aspects of their depression can be closely monitored, previous drugs ‘washed out’ and new medications tried where appropriate. The unit is staffed by psychiatrists, psychologists and nurses who are all aware of, or trained in, the theory and practice of cognitivebehavioural therapy. Twenty-six sessions of cognitive-behavioural therapy are given over a twelve-week period (the mean length of stay on the Newcastle unit was fourteen weeks). Initial sessions are shorter but more frequent (twenty minutes, three times a week) so that the total, one hour per week, is the same as conventional cognitive therapy but split into manageable units. The initial emphasis is on ‘action-orientated’ behavioural work and specific attention is given to engaging the patient in psychological treatment. Each patient has a key worker who coordinates their therapy. Members of staff (not necessarily the key worker) spend periods of five to fifteen minutes at various points during every day seeing the patient, and encouraging them in therapy. Because of shift changes, roles are defined, so that the same people can take on different roles, or different people can take on the same role on different days. There are six roles defined so that each patient will have at least this number of periods of time spent with them each day: 1. Activator: the person in this role, usually the key worker, helps the patient plan their activity schedule for the day. 2. Reinforcer: the person in this role encourages the patient during the day, looking out for when they have achieved a task on their activity schedule.


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3. Motivator: the person in this role deals with those thoughts and experiences a patient may have during the day which make them feel hopeless and that ‘nothing will help them’. 4. Collaborator: the person in this role looks for opportunities to collaborate with the patient in finding ways around difficult problems that occur in carrying out assignments. 5. Observer: the person in this role monitors the behaviour of the person during the day. 6. Evening therapist: the night staff spend a short time with the patient talking over the day (see below). The aim is to remind the patient of positive or neutral things which have happened during the day, which the patient might normally ignore when encoding the events of the day into long-term memory. After three weeks (nine sessions), the frequency of sessions is reduced to two (half-hour) per week. By the end of treatment sessions are scheduled for once a week. Three sessions are scheduled for close family members. The aim is: 1. to explain the cognitive-behavioural approach 2. to involve them as co-therapists 3. to examine their own cognitive distortions about themselves and the patient 4. to encourage them to reduce any negative attributions and behaviours which arise from these distortions 5. to re-integrate the depressed person into their family As soon as possible, inpatients are encouraged to go home for weekends as part of the re-integration with the family, and to encourage the cognitivebehavioural principles to generalize from the ward to the home setting. Comment The fact that eleven out of sixteen patients who experienced this milieu therapy in Scott’s series reported that they were either much improved or back to normal implies that this approach is worthwhile. These were patients with very severe and chronic problems. The cost of the treatment package must be offset against the cost of future inpatient treatment for these people. As with most milieu therapies, the greatest effort is setting them up in the first place. Once in place, nurses typically find that they spend no more time with patients than they did before, but now their time spent with patients has greater purpose. This increases the staff morale, and with it there is more optimism about the possibility of change which communicates itself to the patients and their families.

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Defining the roles to be taken up with respect to each person each day helps to overcome problems associated with shift changes and changes in personnel. Where this is not done, individual staff bear all the responsibility for an individual patient, but when that staff member is off shift or away on leave there is often no one who takes over responsibility. Treatment is then put on ‘hold’ and the patient may well become very pessimistic again. By contrast, the shared responsibility in the Newcastle unit ensured that treatment did not come to a standstill when staff were away or on another shift EVENING THERAPY (Benatov, 1981) Rationale Memory is a basic determinant of consciousness, behaviour and future expectations. Many events each day do not pass the ‘barrier’ or ‘filter’ into longterm memory. This filter is biased negatively in depressed patients so that only depressive events tend to be remembered. This biasing maintains the disorder. Aim of treatment The aim is to redress the bias in what is selected from everyday events to pass into long-term memory. Procedure Time is set aside each evening or at least four times a week. A quiet room and a comfortable armchair (back to therapist) is the setting in which the patient is instructed to recall every detail of that day. Benatov talks of the ‘re-activation of short-term memory’, the aim being to ‘restore STMs of the day in all details’. The patient is led to concentrate on information from ‘perception’ rather than ‘interpretation’. In early sessions, patients tend to begin with an ‘egocentric structure of the facts’, but later are able to pay more attention to all details of daily experiences. Comment This is an interesting procedure which seems to share the aims of realitytesting of cognitive therapy. It is simple in concept, and has, of course, a great deal of experimental evidence to back up its rationale. Depressed individuals do tend to select out the negative feedback. Of course, the terms STM and LTM should not be taken as referring to the same constructs as in most cognitive psychology theories. If so, there would be some difficulty in the ‘recovery’ of material which was supposed to be ‘lost’. Nevertheless it is true that for all people (depressed or non-depressed) remembering everything we


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have done in the last twenty-four hours is difficult, and this common frailty allows a great deal of negative bias to creep in for a depressed individual who can easily believe that a long sequence of unpleasant things has happened to the exclusion of all else. Because it needs to occur daily, if possible, it seems very suitable for inpatient work. The role of therapist could perhaps be played by any one (or more) members of the multidisciplinary team—nurse, psychiatrist, social worker or psychologist (see milieu therapy above).

INTERPERSONAL ISSUES FOR THE CHRONICALLY DEPRESSED PATIENT So far, a number of techniques to use with inpatients or daypatients have been described. A consistent theme has been the need to take account of the family of the patient. There has been a burgeoning interest in the use of cognitive-behavioural therapy in treating relationship problems, such as Beck’s book Love is Never Enough (1988). Readers particularly interested in marital work will find Beck’s book very helpful both for themselves and for their patients to use. In the section which follows I bring together one or two basic behavioural techniques for use when one partner has been severely depressed for a long time. The general aim of such therapy techniques is to improve skills in interacting, and to increase the extent to which patients and partners accept themselves and each other. The particular communication skills to be improved includes the expression of and response to wishes, anger, disappointment, anxiety and positive emotions—happiness, joy, interest, surprise, contentment. Some therapists suggest that a central difficulty for couples is to maintain a balance between distance and closeness. Conflicts often occur when one partner wants more distance and the other wants more closeness. Strategies must be developed for coping with these competing needs. USING PARTNER AS SOURCE OF REINFORCEMENT Rationale Depressive states are associated with a failure to control one’s interpersonal environment (McLean et al., 1973) with the result that adaptive (‘performing’) behaviour is extinguished and depressive behaviour is reinforced (Burgess, 1969). Aim of treatment The treatment aims to reverse (using partner as ally) the progressive extinction of ‘performing behaviours’ and reverse the acquisition/maintenance of

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‘depressive behaviour’. This is attempted by teaching both patient and partner about reinforcement principles, instructing the partner to selectively ignore and reinforce aspects of the patient’s behaviour (Burgess, 1969; Lewinsohn et al., 1969) or by modification of the verbal interaction style between partners (McLean et al., 1973). Procedure Assessment takes place according to principles outlined in Chapter Six at an initial interview. Emphasis is on discovering the things which the patient is not now doing that they used to do; finding out what they used to find most rewarding and which of these activities are still currently available (see Chapter Six); specifying ways in which the depressive behaviours are being inadvertently maintained and reinforced; getting a complete description of symptoms, and a breakdown of any recent life events. Burgess (1969) emphasized to her patients that a major effect of depression was its tendency to inhibit the completion of tasks. These little failures themselves arouse further mood disturbance and also represent an interruption in the smooth flow of behaviour, a disruption which is often socially reinforced (e.g. someone else finishes the task, sympathizes with the patient, etc.). At the most straightforward level, treatment consists of selecting simple, easily executed tasks for which the probability of completion is high, and encouraging the partner to reward completion with attention and praise. Note that in this treatment, the couple is told that successful completion of a task is in itself the goal, and that the nature and value of the task itself does not matter. It is important to encourage the partner to give reward only according to prescribed contingencies—for completion of tasks, not for complaints of how difficult the task is (see Chapter Six for activity scheduling procedures). Burgess gives two examples of patients whose spouses were involved in treatment. Both found the simplest tasks very difficult, showed sleep disturbance and decreased sexual interest, they failed to attend work, had little interest in interacting with others, and ruminated about their own worthlessness and the possibility of suicide. The first was a twenty-six-yearold graduate who, having recently changed his job, was having difficulty adjusting. He blamed all of these difficulties on to his own failures and deficiencies. Task assignment started at the most simple level with making telephone calls, mowing the lawn, drying dishes, etc. and progressed to complex tasks such as job interviews, taking employment tests, and writing CVs. The patient’s wife rewarded him only for completion of a prescribed activity with attention and praise, and ignored the depressive behaviour. Burgess reported very quick improvement (two weeks) although it is to be noted that the patient was seen daily for the first week, thus demanding a great deal of therapist time.


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The second was a forty-year-old sociologist who had recently lost his job and was in the process of selling two properties. Again he was seen daily at the outset His assigned tasks included receiving telephone calls, reading twenty pages of a textbook, eating dinner with the family and keeping a log of tasks performed (time spent, others reactions, his own level of mood disturbance). Husband and wife were subsequently seen together once a week. It seems that instructions to the wife about rewarding, ignoring and coping with depressive behaviour respectively had not been sufficient to change the wife’s negative style towards him, or the family’s reinforcement of his depressive behaviour. Follow-up data suggested that this treatment was producing gradual changes in the desired direction. CONJOINT THERAPY—MUTUAL REINFORCEMENT BY PATIENT AND SPOUSE Procedure Assessment is done by a one-hour session conducted at the outset in the patient’s own home with all the family present (there is a similar session conducted at the middle and end of treatment). During this home session, the behaviour of the patient, and its consequences, are carefully monitored Lewinsohn has produced a manual for how to do this (‘A manual far instructions for the behavioural ratings used for the observation of interpersonal behaviour; unpublished MS, University of Oregon). McLean et al. (1973) adapted these assessments for twenty couples with the following form (see Table 8.2): 1. Instruct the couple to conduct a conversation, at home, about some of their problems, lasting half an hour, and to tape record it (by themselves). 2. Analyse the tape recording by splitting it up into sixty thirty-second intervals. 3. Code the interaction according to whether, during that period, an individual was initiating or reacting to conversation in a positive or negative manner. 4. Average the scores across patient and partner. 5. Express negative interaction score as the proportion of total interaction for each tape session. McLean et al. (1973) report inter-scorer agreement between 73 and 97 per cent (average 88 per cent). Table 8.2 Subcategories of verbal interactions

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Clearly, one can concentrate either on total negative actions and reactions within an interaction, or only on the actions and reactions of the patient. (Lewinsohn then uses the interaction data to define treatment goals. Such analysis following home observation may reveal very one-sided interactions or that the patient does not reinforce behaviour directed at them. It may also become dear that the topics of conversation in the home are of little interest to one or other partner.) McLean et al. (1973) focus explicitly on the relationship. They emphasize to patients the punishment aspect of these interactions, and how, very quickly, depressed behaviour by one partner leads to (and is then further caused by) ignoring or criticism of a behaviour. It is explained how couples often take appropriate behaviour for granted, and reserve feedback for behaviour which is not appreciated. Eventually, the couple may decide that ‘it doesn’t pay to talk about it’ and thus condemn each other to continue to make the same mistakes. Treatment consists of eight one-hour weekly conjoint sessions with male and female co-therapists. At the outset, depression is explained to the couple in social learning theory terms. Three aspects are emphasized: 1. Alienation and apathy can grow up in a relationship over a long period due to the couple not rewarding each other for appropriate behaviour. If one individual does not behave in a way which elicits a positive reaction from the other, a downward spiral in the relationship may begin. 2. As the level of adaptive, appropriate behaviour gets less and less, the couple will tend to turn to coercive techniques to try and produce the desired behaviour. The coercive techniques tend actually to lower the probability of the very behaviour it aims to increase, in the long run. This leaves both partners feeling powerless. (Seligman’s learned helplessness theory is used here to illustrate the wide-ranging effect of such feelings of powerlessness.) 3. Such a sequence of events may lead to cognitive, somatic and behavioural manifestations of depression in one or both partners. In the early stages, there are payoffs for depressive behaviour which reinforce the non-coping behavioural style—sympathy, lessening of criticism by spouse, etc. A ban is put, by the therapists, on ‘blameful’ statements by either partner. The therapists emphasize the importance of avoiding ‘bringing up the past’ to explain or justify the current situation. The differential effect of positive and negative reinforcement on behaviour and emotions is discussed. Emphasis is placed on being specific about behavioural goals each wants to achieve or wants their partner to achieve. The therapy consists mainly of the use of reciprocal behavioural contracts, practised throughout the eight sessions (for further details of this approach see Patterson and Hops (1972)). In this scheme, partners are taught to make


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specific requests about the behaviours they would like the other to change. If it is agreeable to the spouse, each requests the change in the other’s behaviour. An example of reciprocal contracting is given in Table 8.3, from the case of Sarah Jane. Table 8.3

Reciprocal contracts negotiated by Sarah Jane and her husband Jack during marital therapy (Liberman and Roberts, 1976)

Comment Note that Liberman and Roberts were implementing this strategy following Sarah Jane’s progress in making use of behavioural contracts as part of the day unit. It was explained that, though the receipts were very artificial, they at least kept both partners aware of the contractual agreement into which they had entered for the purposes of therapy. It also represented some observable reminder to give more general reinforcement (attention, praise, etc.) to the other. The couple is assured that the receipts will be dropped when both feel settled in the new pattern of interacting. In McLean’s use of this technique, the couple are instructed to comply with their side of the bargain whether or not their own requests are being met, for the first three weeks of the eight-week treatment. Thereafter, they are obliged only to carry out their behavioural target (e.g. coming home on time) if their partner carries out theirs (e.g. dressing attractively).

CONCLUDING REMARKS Most clinical research trials of psychological treatments come to the same conclusion as clinicians who work with depressed patients: that there are

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some patients who respond very poorly, if at all, to psychological treatment. I mentioned at the outset Hollon’s list of factors which are associated with such ‘nonresponse’: high Beck score, current episode longer than six months; inadequate response to previous treatment; two or more previous episodes; other psychopathology apart from depression; impairment across a wide range of psychological functioning; and poor tolerance of stress. But I also pointed out that these (and other chronic factors—most notably a high score on neuroticism) predict poor response to any intervention, physical or psychological. So the conclusion that ‘chronic patients do not respond so well to cognitive-behavioural therapy’ is perfectly consistent with the proposition that cognitive therapy may be better than any other approach for such patients. The therapy will be delivered differently from the standard one hour per week treatment over three to four months. But the studies reported at the start of this chapter, and the techniques detailed in the latter part, should give us hope that some of the most difficult and intractable problems known in psychiatry and psychology may now be treatable: that some people who previously could not be helped may now be able to work alongside their family and therapist to achieve some more lasting progress.

NOTE In writing this chapter, I am greatly indebted to Dr Jan Scott of the University Department of Psychiatry, Newcastle upon Tyne whose pioneering clinical work in this area has given hope to many patients and clinicians where there was little hope before.

Chapter 9

Training exercises

There are probably as many ways to improve one’s skills in therapy as there are trainers and trainees. Whether one is fairly new to the practice of psychological treatment of depressed patients or has a great deal of experience, the improvement of skills remains an important component of one’s job. To some extent we may apply the same model to our own skills as we ask our patients to apply in coping with their lives: we may learn to determine appropriate goods for our therapeutic practice, then decide what strategies will make those goals more likely. Within each general strategy, there will be specific tactics which will be optimal in attaining the desired goals. In order to improve these skills we shall need to do what we require of our patients: to self-monitor, self-evaluate and self-reinforce. The first of these is easy to arrange. We can tape our interactions with some patients some of the time, and it may be useful to be specific in scheduling this into our therapeutic practice. This can be a very revealing exercise. There is often no harsher critic of one’s practice than oneself. On the other hand it has its drawbacks. We may be better at spotting our faults than knowing how to put them right. In this respect, it is often useful to hold group discussions on a regular basis with close colleagues who are grappling with the same issues. Such regular discussions will help the self-evaluation and self-reinforcement aspects of skill development. This section of the book aims to provide some material which individuals or groups may find helpful in their own skills training. Part I contains some case descriptions together with questions to direct the attention to certain aspects of the material. The focus is on determining general therapeutic strategies. Part II becomes more particular, focusing on determining strategies within the therapy session. Part III is similarly specific, but focuses on between-session homeworks, diaries and thought forms. Part IV gives some suggested techniques for role induction, should a group wish to use role-play format as a training exercise. Finally, Part V gives hints on dealing with common frustrations in therapy. None of this material is an adequate substitute for the reader’s own clinical case material. Rather the material included raises issues and illustrates points which may remind individuals and groups of patients they have seen to whom 201

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the same questions could be applied and with whom the course of therapy has raised similar issues. Finally, in reading this material, guard against the assumption that the cases you read are ‘obviously suitable for such and such an alternative therapy’. In many patients, alternative therapies will have been tried, and they are being referred for cognitive-behavioural therapy precisely because the alternatives have not been successful. PART I: DECIDING GENERAL THERAPEUTIC STRATEGY Read the following case descriptions as if you were to decide which therapeutic strategy you would prefer to use. It may be helpful to bear in mind two specific models and compare what further information you would need in order to initiate either. Let us therefore focus on contingency management and reality-testing. What contingencies would you want to manage? What strategies of reality-testing would you employ and what aspects of reality would you seek to test? To what extent do both techniques assume that the objective reality for the patient is benign. If ‘reality’ is genuinely stressful, what follows for your therapeutic practice? Case 1 Stephanie is a twenty-three-year-old woman, who lives with her mother and father in a small private house near the city centre. She is their only child. She did moderately well at school until in her mid-teens when she got bored, and left at the earliest opportunity without taking any exams. She moved from job to job, never settling at anything for very long. She is now unemployed in an area where jobs are scarce, even for qualified youngsters. The home situation has always been tense. Her mother and father have violent arguments. She takes her mother’s part in these—feels she needs defending. Her passion is dressmaking. Although limited by lack of finance she takes great care about selecting patterns and has done some designing herself. Stephanie has always been a loner, but now she has been referred by her GP for treatment of depression. She lacks interest in anything except dressmaking; she cannot get to sleep at night and finds it difficult to get up in the morning. She eats very little. She feels life is not worthwhile and has considered suicide. Recent incident: an interesting-looking job prospect has fallen through. Case 2 John is a thirty-four-year-old man, married with two children, aged six and four. He is referred for treatment of depression of three years’ duration, the

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main characteristic of which is bouts of severe lethargy and depression (lasting two to three weeks) separated by up to a week of feeling ‘perfectly OK’. During these ‘good spells’ he is not ‘high’, and shows no signs or symptoms of mania or hypomania. Antidepressant drug and lithium therapy have had no effect. He was trained as a junior school teacher. The depression came to the attention of health care professionals when he took a large overdose and was admitted to general, then psychiatric hospital. Since then there have been three further overdoses. He has quite a few friends through the children’s school, and through church, but feels he is a burden to them. He often thinks of suicide, and sometimes drives out by himself intending to ‘do something’, but ends up feeling angry that he hasn’t got the courage. ‘They would be better off if I wasn’t there.’ The mornings are especially bad. He is tired, irritable and depressed. The evenings are not much better—he often lies on the couch listlessly, or watches the television without really taking it in. On these occasions he finds it difficult to get to sleep, and the four-year old often wakes them in the night anyway, having recently started to wet the bed. Recent incident: wife went out for night class and children were both ill and bad-tempered. Case 3 Carla is a twenty-nine-year-old unmarried woman who has been referred for psychological treatment of her depression. Before admission to the psychiatric unit she had lived in a flat with workmates (she is a trained physiotherapist). Her work had been punctuated by frequent absenteeism due to unspecified illnesses. She had found work stressful and had several times left the flat to go back to her family home. (Indeed, she had started training at a college away from home, but had returned after only two weeks, and completed her training from home.) She was a ‘good worker’ but her frequent absenteeism meant she could not be given responsibility, and juniors were promoted before her. Her absenteeism increased and she took three moderately severe overdoses during a four-year period. Her mother and father and younger sister still live at home. When she goes home she gets frustrated and her mood is extremely volatile. She feels she has no personality, that she has no ‘guts’ or ‘stickability’. ‘Everyone else is so composed.’ ‘My friends are sick of me.’ ‘I can’t even hold down a job.’ Recent incident: phoned home and parents too busy to talk, on same day as a friend did not keep a coffee appointment.

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Case 4 Patrick was referred for psychological treatment of depression, secondary to bouts of panic and anxiety he had suffered for some time. At the time of referral he had difficulty sleeping, had loss of energy, and increased tiredness, psychomotor agitation, loss of interest in usual activities including social contact and sex, and a diminished ability to think and concentrate. He trained as a veterinary surgeon (the same profession as his father). He took a year out due to excessive anxiety which failed to respond to pharmacological treatment. He moved back to his home town where, as an inpatient he was successfully treated by relaxation methods, after which he moved back to college to finish his training. After qualifying he started to work in his father’s surgery, but missed the college social life and felt isolated in a country practice. He married and moved back to the city in which he had trained. The anxiety symptoms returned and he also became very depressed. He was referred for assessment for individual psychodynamic therapy but was felt to be too overcompliant/ dependent and started in group psychotherapy instead. He felt uncomfortable with this arrangement and discharged himself after a few weeks, after which he was referred for cognitive-behaviour therapy. Recent incident: wife, who has been very supportive up until now, says she is getting tired of his behaviour. He feels she may get bored with him and leave. PART II: CHOICE POINTS WITHIN THE THERAPY SESSION When you listen to a tape of your therapy sessions you may be able to identify various points during the session where the course of therapy could have travelled in a number of directions. It becomes an interesting exercise for a therapist (perhaps with a group of colleagues) to listen to a tape and identify these choice points. Once these have been identified, you may discuss the range of options and why one was chosen rather than another. In this way, group members can sensitize themselves to the process of therapy interchange. In the transcript that follows, I have cut up the session. At each stopping point, the reader may consider which way they would have directed the session, or whether they would have attempted to allow the patient to decide. If you are doing this exercise in a group, each member may first make their decision, after which differences in members’ conclusions may be discussed. If you find this particular transcript is not satisfactory for your group’s needs, use one of your own tapes or transcripts and stop it at various intervals to try the same exercise. The transcript extracts which follow were from a twenty-two-year-old man who had been depressed since his final year at school. He had then given up his A level course but had now gone back to a technical college to do some less

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advanced exams—to ‘get back into the swing of it’. By the time this session was held, considerable progress in therapy had been made, though the patient believed this was due to a ‘biochemical depression’ which had now lifted. The therapist was concerned to investigate the patient’s attribution of his success (biological factors vs learning coping strategies) in order to discover his level of vulnerability to possible future stresses. The patient believes that everything he has achieved has been really quite easy since his biological depression lifted. What would your strategies have been at the choice points I have indicated? Therapist So this is what you filled in two weeks ago. And we were doing this to see what activities you are involved in now. (Patient brought in two weeks’ activity schedules.) Patient Well I think it was to compare with the one I did right at the beginning. Therapist That’s right. Yes. Patient I don’t know how accurate the times are, because I tended to find I got to the end of the day and couldn’t remember. Therapist So you were filling it in at the end of the day retrospectively. It seems a lot busier, a lot more full than the other one we had, which we’ve got here (earlier activity schedule). The pleasure scores are quite high as well. Patient Some are, some aren’t, it depends. Therapist There are quite a few over 5, 5 out of 10. Patient Oh yes. Therapist Before you were finding things had little pleasure, or enjoyment, is that right? Patient I think some did, probably not everything. Choice point Therapist How’s it been about getting up in the morning? Patient OK. Therapist What sort of times have you been getting up?. Patient Well it depends what time I have to get up. If I’m going to college for nine, I get up around seven. Therapist And is there any problem getting up at seven? Patient No. Therapist You don’t find the old problems creeping back of lying in bed, thinking about getting up and not being able to do it, putting it off. Patient Not if I have to go to college for nine. If, say, I don’t have to go until the afternoon, sometimes I do. Therapist What sort of thoughts do you have, if you’ve got college at nine; when you wake up, what thoughts run through your mind then? Patient Just that I’m going to college and I have to get up, and that’s it It isn’t really all that difficult actually. Choice point

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Therapist How do you actually get up, how do you decide to get up? If you’re thinking—there’s nothing to get up for, it doesn’t make any difference what time I get up, so I might as well lie in a bit longer—where does the change come before you actually decide to get up? Patient Possibly in the time. If it gets toward ten o’clock—I feel I ought to get up. Therapist Um—so as it’s getting later you feel slightly obliged? Patient Yeah. Therapist And that time’s about ten o’clock. Patient Yeah. Therapist Whereas before you were saying it could be midday, one o’clock in the afternoon, that you were lying in till, and you still didn’t want to get up. Patient Yes, but I still might not want to get up at 10 o’clock. Therapist But you do. Patient But I do, yes. Therapist So that’s a big contrast, isn’t it? Patient Also I think, possibly, there are more things that I want to get done. Therapist There are more things to get up for? Patient Mmm. Therapist Can you give me an example of what some of those things are? Patient Uhm, well I might have essays to write, I might have a book I’ve started, or I haven’t taken the dog out—which I could put off, but the more you put them off, there’s probably things that I’d want to do then anyway. I suppose there’s less empty space. Choice point Therapist Yes. So some of the things are the same things that you used to do before which seem to have a bit more meaning, like walking the dog or reading, they were the sort of things you were doing beforehand but you couldn’t be bothered so much about. Patient Yes, I think I could put them off longer. Therapist And other things that you are doing are actually new things, that are part of your life now, that weren’t before, to do with college. And they actually encourage you to get on with the day? Patient Well I have to get them done, so—yes. Choice point Therapist It seemed, at one stage, when we were talking about the problem of getting up, that you thought you believed it to be insurmountable, and that there was no way round it. Patient It depends on how I was feeling. If I was feeling very depressed, I think I would still see it like that But I feel alright. Therapist So you’re saying that when you’re OK, when you’re not depressed, it’s not a problem. But if…

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Patient If I became depressed, it wouldn’t bother me, not going to college, it wouldn’t be worth getting up then. Therapist So there’s always the chance, that if you become depressed, it all might shatter again. Patient It might. Therapist And you might be back at square one? Patient Possibly. Choice point Therapist What could you do to stop that happening? Patient I don’t know. Therapist How have you stopped it happening in the past? Patient You can ignore it. Therapist So you just put up with it and carried on. Patient I tried to for a while. Therapist And then what makes it change? Patient I start doing more. Therapist And what makes it change when you start becoming better and start being more active, like you have done in the last six weeks? Patient I start feeling better and I start wanting to do more. Therapist So your mood improves. Patient Yes and that makes me feel like I want to get up and do something. Therapist Does it ever work the other way round? That you do something and that makes your mood improve? Patient Don’t think so. Maybe a little bit. Not to a great extent. It certainly feels like I don’t have any control. I mean, I can sort of manipulate it—if I feel a little bit depressed I can ignore it or do something I like, things like that. But if I’m going to get really depressed, I don’t think there’s anything I can do. Choice point Therapist How did you feel when we set the first target of getting up, in the mornings at nine o’clock? Do you remember when we set that first target five weeks ago and beforehand you were having the problem of staying in bed indefinitely throughout the morning and rising fairly late morning or early afternoon? Patient Uh-huh. Therapist You had quite a lot of negative thoughts about that. Patient Uh-huh. Therapist But you did try and do the target, and you succeeded, didn’t you? Patient Mostly. Therapist In the majority. Patient Yes.

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Therapist So how does that make you feel about how much control you have over what happens to you? Patient But it still wasn’t a very big target. And, I wasn’t all that depressed at the time. Choice point The session continues with discussion of the extent to which the decision to go to college has helped his motivation to do other activities. The therapist then reviews another area the patient had found difficult. Therapist Yes—how do you find your decision making is generally, because that was something that used to worry you, wasn’t it? Patient Yes, it’s OK. Therapist It’s improved? Patient Yeah. Therapist In what sort of ways? What sort of things are easier to decide about? Patient Well, I can’t think of anything that’s not improved, but I mean I haven’t had any major decisions to make. Therapist No, but it was small decisions that were… Patient Everyday things are alright. Therapist Yes, it was the everyday decisions that were difficult, weren’t they? Patient Yes. Therapist What do you put that down to? What do you see as being… Patient Feeling better, not feeling depressed. PART III: STRATEGIES FOR BETWEEN SESSION THOUGHTCATCHING In this section, samples from patients’ thought-diaries are presented. Look particularly at the differential effectiveness of the ‘rational response’ category in alleviating the original emotional disturbance. Why do these responses sometimes work and sometimes not? A possible reason may be that the ‘rational response’ represents a ‘vain hope’. If there is no evidence for the rational response the optimism is empty and may not effectively challenge the validity of the negative thought (e.g. 1, 3). A second possible reason is that the rational response represents a ‘must’ or ‘ought’ or ‘got to’ statement which merely increases pressure on the patient (e.g. 8, 9). A third important variable is degree of belief in the response (e.g. 7). In each case the intensity of emotion and degree of belief are rated on a 1–100 scale where high scores represent greater disturbance and greater belief, respectively. 1. Situation: Watching holiday advertisements on television – Emotion: Hopeless (80)

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– Negative thought: I’ve been in this mess for a year—I’ll never travel again (95) – Rational response: I managed to cope before. I could do it again (20) – Emotion: Sad (50) Situation: Watching group of students talking – Emotion: Sad (100) – Negative thought: I don’t think things will ever be the same again (60) – Rational response: Things are gradually getting back to normal. Just wait a little longer (80) – Emotion: Sad (50) Situation: Trying to plan day, one morning – Emotion: Frustration (80) – Negative thought: My friends are all living their own lives and I can’t break out of this prison (80) – Rational response: This time next year my life will be moving again (20) – Emotion: Frustration (80) Situation: Just returned from evening with friend – Emotion: Sadness (100) – Negative thought: I hate being myself, I wish I could escape (50) – Rational response: This is just reaction against knowing I must change (70) – Emotion: Sadness (50) Situation: Waking up (in dressing gown) – Emotion: Despair (80) – Negative thought: This is going to go on forever. I wish I were dead (40) – Rational response: I recognize this early morning feeling. It will go on for the next hour at most (80) – Emotion: Anxiety (50) Situation: Thinking about old friends – Emotion: Loneliness (80) – Negative thought: I’ve made a terrible mess of my life (90) – Rational response: I’ve made a mess of the last year, perhaps (10) – Emotion: Loneliness (70) Situation: Drinking with friends – Emotion: Rejection (80) – Negative thought: I feel distant from those around me. People can’t like me (40) – Rational response: I’m expecting too much attention (unrated) – Emotion: Rejection (80) Situation: Thinking about my situation – Emotion: Hopelessness, despair, feeling of failure (90) – Negative thought: There’s no way out. There’s no reason for

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continuing. I’m tired of struggling to keep up appearances. I’d like to just drive away (95) – Rational response: I’ve got to keep trying to overcome this (60) – Emotion: Hopelessness—worse because I can’t think of a rational response (95) (I know what to do but seem unable to do it) 9. Situation: In office, sitting looking busy but not working – Emotion: Despair (100) – Negative thought: I am a burden to my husband, children and everyone (100) – Rational response: I must attempt to get back the fight—the will to survive (unrated) – Emotion: Continuing desperation (100) Now you have read them through, how useful do you think the technique was with these patients? What do you think accounted for the difference in effectiveness of rational responses? To what extent are the rational responses only helpful when they represent attempts to modify the factual basis of the negative thought (e.g. 5, 6)? Finally, consider the following sequence: – Situation: At home, sitting thinking – Emotion: Nervy, anxious (70) – Negative thought: I’m getting hooked on my pills. Joan (friend) said last night ‘once you’re on pills, you’re lost’. I always used to think like that (70) – Rational response: (I hate doing this bit; it makes me feel worse) 1. I’ve mown the lawn today and talked to three interesting people 2. I’ve made dinner, and done some reading—the normal things of life (20) – Emotion: (unrated) (I find it difficult to think of rational responses. When I do, I don’t believe them. It’s very demanding.) Why might this patient be finding it so difficult to generate rational responses? How representative of your own patients is this patient? At what point would you want to give up this approach and try an alternative strategy? What alternatives would you consider? (For a discussion of some aspects of this problem, see p. 159.)

PART IV: TECHNIQUES FOR ROLE INDUCTION FOR TRAINING WORKSHOPS As in the course of cognitive behaviour therapy, so in training in therapeutic skills, the use of role-play is often beneficial. On many

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occasions it will be sufficient for a group to assign therapist and patient roles to two of its members, using pen portraits such as those in this chapter or other case histories. Occasionally, however, the group may wish to concentrate more attention on getting into the role of the patient—to attempt to experience something of the feelings that depressed patients feel. There is now an extensive research literature on mood induction procedures (see Goodwin and Williams, 1982; Clark, 1983), and in this section I want to describe two such procedures in enough detail to be usable in the role induction context. Specifically, I suggest that half the members of a group use the mood induction procedures to induce the role, which, together with some preprepared biographical outline, will form the basis of their role-play of the patient. The other group members, the therapists, have access to the biographical information, but are not present at the mood induction. Therapists have prepared instructions to conduct, for example, an ‘initial session’ (in which part of their agenda will be to explain the principles on which therapy will be based), or to focus on explaining and using a particular technique. Role-plays are then conducted in pairs, with the group coming together again after a predefined interval to discuss their sessions. At other training sessions, the roles may be reversed. Mood induction I—Negative self-statements The following is a list of negative self-statements of the type used in mood induction research. They are divided into self-devaluative statements and statements reflecting somatic concern or fatigability. You may select some from each list or use each separately. Select twenty to thirty items and type each on a card. The procedure for mood induction has varied from study to study, but a powerful procedure is for the ‘subject’ to study the cards, one by one, spending longer on the statements which are felt to be particularly meaningful and less on those which are not felt to be disturbing or appropriate. Continue this for seven to eight minutes, if necessary looking through the statements for a second time. The individual is encouraged to identify with the mood associated with the statement. Some biographical detail will have to be supplied before or after the role induction procedure. For example: You are a thirty-three-year-old mother of three children. Your husband works shifts in a factory. The money is adequate but the shift times are inconvenient, and leave you having to look after the house and children without much support. (Coming off shift-work would mean less money.) Recently you have lost contact with several friends, and lost interest in hobbies inside and outside the home. Things look very hopeless. Here is the list of self-statements:

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1. Somatic statements – Other people seem so much more lively than I am – I really can’t be bothered to do anything – I don’t feel very energetic – My whole body feels worn out – I do feel ready for a good rest – I do seem to get tired very easily – I feel heavy and sluggish – It seems such an effort to do anything – The mere thought of exercise is appalling to me – I feel as if it would take me twice as long to do anything – I feel so tired that I would rather just sit than do anything – I haven’t even the energy to keep a conversation going – I just can’t make the effort to liven myself up – I just feel drained of energy, worn out – I feel as if my whole body has been slowed down – I feel as if I haven’t had a proper sleep for a week – I don’t think I could exert myself even if I wanted to – I’m so tired I don’t want to do anything at all – I just want to curl up and go to sleep – I feel absolutely exhausted – Sometimes it’s just too much effort even to move – I’d like to go to sleep for a very long time – I’m so tired, my thoughts keep drifting away – I have to really concentrate to keep my eyes open – I’m having difficulty stopping myself from just falling asleep – I feel absolutely shattered 2. Self-devaluative statements – I have too many bad things in my life – I often wish that I were somebody else – I have very little to look forward to – I am less successful than other people – I feel disappointed the way things have turned out – I don’t get much pleasure about being with my friends – I am annoyed at myself for being bad at making decisions – I don’t think I make a good impression on other people – I’m not too hopeful about the nature – I don’t get the same satisfaction out of things these days – There are things about me that I don’t like – Everything I do seems to turn out badly – I regret some of the things I’ve done in the past – I know I’ve made mistakes in my life – I’m very aware of my faults – I often feel ashamed of things I’ve done

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There are things about me that aren’t very attractive Some people don’t have a very high opinion of me Life seems boring and uninteresting I feel lonely and isolated The future seems just one string of problems I’m miserable, and there’s no way for things to get better

Mood induction II—taped depression story The following story, developed by D.Rosenhan and his colleagues at Stanford in their studies on affective determinants of altruism, is also a powerful mood induction procedure (Williams, 1980). It is tape-recorded, and played to the ‘subject’ who is asked to identify with the story. As with the self-statement role induction, the person role-playing the patient will need to be given some biographical detail, following the mood induction, onto which the disturbed effect may be ‘attached’. For example: It is now three months after your friend’s death. You have become tired and listless, and lost interest in your work. You don’t go out much now, and your former hobbies are of no interest to you whatever, even the thought of them makes you feel drained of energy. You are thinking of giving up college, but on the advice of your tutor, have come to see a psychotherapist, though you doubt it will make any difference. Here is the mood induction story: Sit back, and close your eyes. Relax. Let yourself sink into the chair. Focus all your attention on my voice. Let yourself relax and become absorbed completely in the things I am telling you. What I would like you to do is use your imagination. Put yourself into the situation I will describe. Feel the same feelings. Think the same things. Experience the situation as if you were in it. Let yourself relax and react to your feelings. Picture the events happening to you. See yourself going through them. Try to create in yourself the emotions and thoughts that I describe to you. Imagine that you have a very good friend who is attending college with you. Imagine that you and your friend are very close—and that you like and respect her a great deal. When things go well in your friend’s life you are happy for her, and when things go badly, you suffer nearly as much as she does. You and your friend have been through a lot together, and that has helped you to get to know each other very well. Lately, you’ve become aware that your friend has not been feeling well. She’s been dragging around—not doing much of anything. She seems to have lost her enthusiasm for coursework, and has become grumpy and irritable. She’s really annoying, and you’re upset because you don’t know what’s wrong. One day she confides

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in you that she’s been having a chronic series of headaches and has not felt well for almost two weeks. You are afraid that she might really be sick. At your urging, she goes to the student health centre, but the doctors there find nothing wrong with her, and suggest she might just be overworked. Taking the doctors’ advice, your friend drops two of her courses, and cuts back on all of her extra-curricular activities. But this does not help. As several days go by, you notice that your friend seems to have less and less energy and her headaches become increasingly severe and frequent. She looks terrible, and she’s always irritated with you. Finally you convince her to return to the health centre and this time the doctors take her complaints more seriously. When your friend doesn’t come back from the health centre after three hours you call the centre to see if she’s still there, and learn that your friend has been taken to the hospital where the doctors want to perform a series of tests immediately. The next evening you go to visit your friend at the hospital during visiting hours and to your surprise find your friend’s parents in the waiting room outside her ward. They’ve driven up from their home that morning. They look keyed up and anxious. You realize that there must be something really wrong with your friend. They don’t know what the problem is yet, but the doctors’ tests have eliminated all but the most serious possibilities. You think back, and remember all the good times you and she have had together. They all seem so far away. It hurts you to see her so ill, but it hurts even more to think that those good times may never come again. As the next few days pass, you live with constant depression, trying to be near a phone, spending all your spare time at the hospital and hoping for some change. You think of all the worst things that could happen. She could die and you would lose her, never be able to talk to her again. Or worse, she could die slowly. Every minute with her could be your last time together. For months you would have to be cheerful for her while you were sad. You would have to watch her die in pieces, until the last piece finally went and you would be alone. You know the tests are getting more painful. The spinal tap. The bone marrow extraction. The test in which she has to swallow a radioactive solution that leaves her ill for days. No one has said it yet, but as every other possibility gets eliminated, you come to suspect cancer. That’s a thought you don’t want to have. It would hurt too much to lose her. Only old people get cancer—not people you know. It’s often a long and painful disease with no cure. So you think; and worry; and try and keep it out of your mind as the tests continue. Finally, the uncertainty ends. The doctors determine that your friend has lymphoma, an incurable cancer of the lymph nodes. Your worst imaginings are now real. You are despondent and shocked. She has a year or two to live at most, and her death will be slow and painful.

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You feel that it’s so senseless and so unfair to end this way—she will be gone so fast. All the time you spent with her—all the crazy plans you made together are over. She will leave you alone; and constantly asking yourself what went wrong. You can feel some empty space inside you that will take a long time to fill. But the thought is too much to bear. You are hurt, and helpless, and upset that you will lose someone dose to you to a disease that is so arbitrary and cruel. Note: When the story is taped, the friend may be male or female.

PART V: TROUBLESHOOTING Psychotherapy with people who are depressed is emotionally demanding. Cases reported in the literature almost invariably recover marvellously. Your own patients may seem more reluctant to show such miraculous change. Furthermore, if you have read the outcome literature, you will have in your mind some impressive looking graphs, with smooth slopes heading gently downwards from left to right. Yet these are averaged results, and not a single patient in any outcome trial necessarily follows that pattern. Most patients at several points say they are ‘back to square one’. On such occasions it is difficult not to feel at least a little guilty for not helping them, angry, depressed and hopeless about their prospects. It is difficult at that moment not to think ‘if only I was more skilled, I’d know what to do’. Of course, experience will help: but one of the most important things that it will help with is learning to accept the setbacks, rather than responding to them by giving up. So how can one learn to accept the setbacks? First, by preparing both yourself and the patient for them. Remind yourself and your patient that the course is not smooth and that the ‘back to square one’ feeling will occur. Second, by setting up therapy at the outset to focus on some specific problem which both you and the patient agree needs to be solved. Solutions will not come easily and the setbacks are often opportunities to learn exactly what the difficulties are. Which were anticipated, which were not? Separate the two. But bring the discussion back to the specific problems to be solved. Keep in mind that if the formulation was accurate, solving these problems will indeed have a beneficial effect on mood, but this will take time. Third, you may find it helpful to use assessment instruments (such as the Beck Depression Inventory) regularly, at the start of each session. If this is too long, work together with the patient to select some of the items which seem most relevant, and compile your own ‘short form’ for regular use. Then you can map the score on to a graph such as that shown on page 94. Finally, a hint about what to do when feeling completely lost in therapy. When this happens, try summarizing what has been said, as a prelude to obtaining further information. If possible, make what has been said into the

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first of a list of things. So, for example, if someone says: ‘I feel completely useless, everything has fallen apart this week’, you may ask ‘What has happened this week which has made you feel like this?’ If only one thing emerges (e.g. ‘My husband threatened to leave’) there may seem nowhere else to go in the therapy session. In this case it is nevertheless important to ask if anything else has happened which has contributed to this feeling (there may be something even more significant that you might miss if you do not). Continue asking whether there is anything else until the list has come to an end You will then have a much better notion of where it is important to start. Sometimes there will not seem to be many events in the list, and then it may be possible to return to the initial expression, ‘I feel completely useless’, and make this feeling into the first of a list. For example: ‘You said that when this happened, you felt completely useless. Did you have any other reactions?’ This may then show that the person did indeed have other reactions such as anger and hopelessness or suicidal feelings. When this list is complete, you will again be in a better position to discover which of these thoughts and feelings was the most upsetting. The inverted arrow technique (page 172) may be used to discover more information, or talk about other things that the husband has threatened, or other things that have made her feel this hopeless. You may talk about how to cope, based on what has worked in the past. In any event, gaining more information and listing the situations or listing the feelings deals with the therapist’s own feeling of being completely stuck. Containing their own feelings of hopelessness on behalf of the patient, will allow the therapist to maintain a problem-solving attitude which can encourage the patient. I believe myself that this is because such listing, though it elicits more negative information, can allow a slight distancing to be attained from the problems that are being listed. It may also give the patient the idea that their problems are not infinite—the list has an end.

IRRATIONAL BELIEFS OF THERAPISTS It is worth becoming aware of the beliefs and ‘oughts’ that you have as a therapist. There are many of these which will affect how you feel about your patients. You may find it helpful to discuss these and other beliefs you have about yourself as therapist in training groups with other therapists. It will be helpful then to analyse the common problems in therapy that you share. The sorts of beliefs that therapists may have are as follows: 1. 2. 3. 4.

I have to be successful with all my patients. If I fail, it is because I don’t know enough. Every session must go well. It is my responsibility to make the patient feel good.

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I have to be respected and loved by all my patients. I must be a better therapist than anyone else. As therapist, I should always know what to do in therapy. I should not have any emotional problems of my own. I must not dislike my patients. My patients must never see me make a mistake or misjudgement.

In your training groups you may find it useful to include this sort of idea while discussing other problems that occur in therapy that all therapists share. These problems tend to fall into three categories: characteristics of the patient, characteristics of the patient’s situation and the management of the session. If you find that problems occur in therapy, you are not alone. Discuss with colleagues or your training group what alternative ways may exist to cope with them. Rehearse some of these alternatives. Become aware of how these difficulties are exacerbated by the thoughts they create and the assumptions they activate in you as therapist.

Chapter 10

The cognitive theory of depression revisited

Although it was not until the late 1960s and 1970s that experimental clinical psychologists started seriously to develop theories about the onset and maintenance of depression, even from these early theoretical writings there emerged a controversy about the necessity to postulate cognitive mediators. There are two forms of this debate, the first, with which we shall not be concerned here, is the philosophico-theoretical issue about the status of ‘private events’ and their explanatory power. The other debate is that between those who believe that cognitive events precede and cause the emotional disturbance, and those who believe that the emotional disturbance can be explained on other grounds (biological or behavioural) and see cognitive distortions and negative self-talk as a product or correlate of the emotional disturbance. Now this debate is crucial. If cognitive events are an epiphenomenon, accompanying though not playing a causal role in affective disorders, it would make less sense to devote years of research to how best to change cognitive styles or habitual self-talk strategies. Like ointment on a chickenpox rash, such treatment may soothe but have little prospect of treating the underlying disorder. Of course cognitive therapies do work (see Chapter Four ) but it may be that they are inadvertently affecting other more significant subsystems. Let us then examine the status of the aetiological cognitive thesis. Just to complicate matters further there are also two forms of the aetiological thesis. Let us call them the ‘precipitation theory’ and the ‘vulnerability theory’. The first is a ‘state’ theory and argues that moment-tomoment fluctuations in mood may in part be accounted for by the thoughts, images, and memories that occur to the individual. Controlling the nature, frequency or intensity of these thoughts and images will thereby affect the mood that is consequent upon them. The vulnerability theory argues that long-lasting styles of thinking (e.g. attributional style, tendency to selectively abstract or think dichotomously) occur prior to and render a person vulnerable to depressive breakdown in the face of stress. Although often confused under the general title of cognitive theory of depression, these theories are quite 218


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distinct and ought to be discussed separately. We shall consider the evidence for each in turn.

THE PRECIPITATION THEORY There are two types of evidence in favour of the theory that thoughts and images may precipitate moment-to-moment fluctuations in mood. The first evidence comes from studies of experimentally induced mood. These studies provide particularly useful evidence because, using experimental manipulation of mood, they can eliminate other variables which might otherwise be important contributory factors to disturbed mood (e.g. individual differences). The second type of evidence comes from experiments which attempt to reduce the frequency of negative thoughts in depressed people, and observe the effect of so doing on their mood. Mood induction research Six forms of mood induction procedures (MIPs) have been used. Self-referent mood statements are the most widely used MIP. First described by Velten (1968), the method involves reading aloud sixty negative self-referent statements, e.g. ‘I’m discouraged and unhappy about myself’ or ‘I feel worn out, my health might not be as good as it’s supposed to be’. The statements progress from relative mood neutrality to dysphoria, the overall tone being that of indecisiveness, tiredness, unhappiness, inefficiency and pessimism. Investigators agree that this general procedure is a potent manipulator of mood, as assessed by visual analogue scales (e.g. Teasdale and Fogarty, 1979), the Depressive Multiple Adjective Checklist (e.g. Hale and Strickland, 1976; Brewer et al., 1980), the Personal Feeling Scale (e.g. Frost et al., 1979), and the Wessman and Ricks’ Elation vs. Depression Scale (Coleman, 1975). Furthermore, independent ratings of general demeanour and ‘mirth’ outside the experimental situation (just having completed the experiment) have been found to differentiate between MIP and control groups (Coleman, 1975). The Autobiographical Recollections Method was used by Brewer et al. (1980) in a comparison with Velten’s MIP and various control conditions. Subjects were asked to dose their eyes and recall three autobiographical moodevoking events that made them feel lonely, rejected, defeated or hurt The entire MIP lasted eleven minutes, the three events being spaced in time according to prerecorded instructions. Subjects had to try and recall three events which were progressively sadder and more unpleasant. The results showed that this method strongly affected mood, giving more affective disturbance on the DACL and Beck Depression Inventory than the Velten MIP. Spielberger State Anxiety scores were also affected by this MIP.

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A taped depressive story has been developed as an MIP by D.Rosenhan and colleagues at Stanford, and subsequently modified for use with a British population by myself (Williams, 1980) (Chapter Nine). The taped story, with which subjects are asked to get involved, lasts approximately ten minutes. It asks the subject to imagine a friend becoming ill and eventually being diagnosed as having incurable lymphoma. The tape focuses on the subjects’ own feelings of helplessness and loneliness. I found that this MIP significantly raised anxiety, despondency, irritation and frustration levels, and significantly lowered relaxation and happiness levels, when compared to a control condition. Failure feedback has been used in a large amount of research on the learned helplessness and test anxiety phenomena. These have been comprehensively reviewed elsewhere (e.g. Abramson et al., 1978; Weiner and Heckhausen, 1972). Although most studies have not aimed solely at manipulating depressed affect, many of the studies reviewed by these authors report affective changes following failure experience, or exposure to non-contingency. Hypnosis has been used by Gordon Bower in his studies of statedependent mood-memory effects. He asks subjects under hypnosis to induce a sad mood by imagining an episode in which they had been grievously sad. If they could call up no such scene from their life, the experiment helped them construct an imaginary one that ‘would have the intended emotional impact’. Subjects were told to adjust the emotion until it was intense but not unbearable. Bower et al. (1978) report that their sad subjects were long-faced, morose, slow to respond, and often on the verge of tears. No objective measure of mood intensity was taken, nor any subjective ratings by the subject used, so it is difficult to establish just how effective the procedure was. Bower et al. used only subjects who had demonstrated good hypnotic facility, which, although suggesting that the mood induced would have been subjectively intense, is also a drawback in generalizing from these results. Finally, several investigators have used music as a mood induction procedure (e.g. Sutherland et al., 1982; Teasdale and Dent, 1987; see Clark (1983) for a review of the procedures involved). Sutherland et al. gave subjects a choice of music selected as having sad associations. They found the MIP more successful than that of Velten in changing subjective ratings of anxious, sad and happy moods, though ratings of ‘apprehension’, ‘despondency’ and ‘tiredness’ were not affected. Over the years, Teasdale and colleagues have increasingly used musical induction in preference to the Velten technique in their studies of the effect of mood on information processing (e.g. Clark and Teasdale, 1985; Teasdale and Dent, 1987). In this procedure, subjects listen to a depressing piece of music (‘Russia under the Mongolian Yoke’ by Prokofiev). This music is played at half-speed for seven minutes, and subjects are instructed to try hard to get into a depressed mood. An indication of the size of the effect produced by this procedure can be seen in the group of ‘never depressed’


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subjects (N=21) who took part in the Teasdale and Dent experiment. On a 100-point visual analogue scale labelled at 0, ‘I do not feel at all depressed/ anxious/happy’, and at 100 ‘I feel extremely depressed/anxious/happy’ subjects changed from 2 to 24 on depression (t=3.62, p

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